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  • 1. Bemark, Mats
    et al.
    Friskopp, Linda
    Saghafian-Hedengren, Shanie
    Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut, Avdelningen för immunologi.
    Koethe, Susanne
    Fasth, Anders
    Abrahamsson, Jonas
    Sverremark-Ekström, Eva
    Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut, Avdelningen för immunologi.
    Andersson, Bengt A.
    Mellgren, Karin
    A glycosylation-dependent CD45RB epitope defines previously unacknowledged CD27(-)IgM(high) B cell subpopulations enriched in young children and after hematopoietic stem cell transplantation2013Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 149, nr 3, s. 421-431Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The immune system is dysfunctional for years after hematopoietic stem cell transplantation (HSCT). A potential cause is an intrinsic B cell deficiency. In a cohort of pediatric HSCT patients few CD27(+) B cells formed after transplantation with the number of CD27(+)IgM(high) cells more affected than class-switched ones. A previously unacknowledged population of CD27(-)IgM(high) cells made up the majority of B cells and this population was also enlarged in healthy children compared to adults. Only a minority of these CD27(-)IgM(high) B cells expressed markers typical for transitional B cells, and the non-transitional CD27(-)IgM(high) cells could be further divided into subpopulations based on their ability to extrude the dye Rhodamine 123 and their expression of CD45RB(MEM55), a glycosylation-dependent epitope. Thus, we define several novel human CD27(-)IgM(high) B cell subpopulations in blood, all of which are present in higher frequencies and numbers in young children and after HSCT than in adults.

  • 2. Brännström, Johan
    et al.
    Hässler, Signe
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Peltonen, Leena
    Herrmann, Björn
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Klinisk bakteriologi.
    Winqvist, Ola
    Defect internalization and tyrosine kinase activation in Aire deficient antigen presenting cells exposed to Candida albicans antigens2006Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 121, nr 3, s. 265-273Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Patients with Autoimmune polyendocrine syndrome type I (APS I) present with multiple endocrine failures due to organ-specific autoimmune disease, thought to be T-cell-mediated. Paradoxically, APS I patients suffer from chronic mucocutaneous candidiasis. The mutated gene has been identified as the Autoimmune regulator (AIRE). Aire is expressed in medullary epithelial cells of the thymus and in antigen presenting cells in the periphery. T cells from Aire deficient mice and men displayed an enhanced proliferative response against Candida antigen in vitro, suggesting that Aire deficient T cells are competent in recognizing Candida albicans. In contrast, monocytes from APS I patients displayed a decreased and delayed internalization of zymosan. Furthermore, Candida antigen activated monocytes from APS I patients show decreased and altered phoshotyrosine kinase activation. In conclusion, Aire deficient APCs have a defect receptor mediated internalization of Candida which affects kinase activation, likely altering the innate Candida immune response.

  • 3.
    Chéramy, Mikael
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Skoglund, Camilla
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    Johansson, Ingela
    Linköpings universitet, Institutionen för medicin och hälsa, Kardiologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärtcentrum, Kardiologiska kliniken.
    Ludvigsson, Johnny
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Hampe, Christiane S
    University of Washington.
    Casas, Rosaura
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Pediatrik. Linköpings universitet, Hälsouniversitetet.
    GAD-alum treatment in patients with type 1 diabetes and the subsequent effect on GADA IgG subclass distribution, GAD(65) enzyme activity and humoral response2010Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 137, nr 1, s. 31-40Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We have previously shown that two injections of 20 mu g GAD-alum to recent onset type 1 diabetic children induced GADA levels in parallel to preservation of insulin secretion. Here we investigated if boosted GADA induced changes in IgG1, 2, 3 and 4 subclass distributions or affected GAD(65) enzyme activity. We further studied the specific effect of GAD-alum through analyses of IA-2A, tetanus toxoid and total IgE antibodies. Serum from children receiving GAD alum or placebo was collected pre-treatment and after 3, 9, 15 and 21 months. At 3 months a reduced percentage of IgG1 and increased IgG3/IgG4 were detected in GAD-alum treated. Further, IA-2A, IgE and tetanus toxoid antibodies, as well as GAD(65) enzyme activity, were unaffected confirming the specific effect of treatment. In the GAD-alum group, higher pretreatment GADA were associated to more pronounced C-peptide preservation. The induced IgG3/IgG4 and reduced IgG1 suggest a Th2 deviation of the immune response.

  • 4.
    Garwicz, Daniel
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Palmblad, Jan
    Fadeel, Bengt
    Normal levels of constitutive and death receptor-mediated apoptosis of peripheral blood neutrophils from patients with chronic idiopathic neutropenia.2007Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 122, nr 3, s. 349-355Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    To investigate the role of neutrophil apoptosis in the pathogenesis of chronic neutropenia, we examined constitutive and death receptor-mediated apoptosis ex vivo of peripheral blood neutrophils obtained from six chronic idiopathic neutropenia (CIN) patients and six healthy adult blood donors. Apoptosis was quantified based on phosphatidylserine externalization and caspase-3 activation in freshly isolated neutrophils or after overnight cultivation of neutrophils in the absence or presence of pro- or anti-apoptotic factors, including the pan-caspase inhibitor, zVAD-fmk. Neutrophils from CIN patients receiving treatment with granulocyte colony-stimulating factor appeared to be more prone to constitutive apoptosis than cells from untreated patients; however, further investigations in larger cohorts of patients are needed to validate these pilot studies. Overall, the level of neutrophil apoptosis was similar in patient and control groups, thus supporting the notion that the underlying defect in these neutropenia patients lies elsewhere, such as in the bone marrow microenvironment.

  • 5.
    Grönwall, Caroline
    et al.
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden..
    Hardt, Uta
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden..
    Gustafsson, Johanna T.
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden..
    Elvin, Kerstin
    Karolinska Univ Hosp, Karolinska Inst, Dept Clin Immunol & Transfus Med, Unit Clin Immunol, Stockholm, Sweden..
    Jensen-Urstad, Kerstin
    Karolinska Inst, Dept Clin Physiol, Sodersjukhuset, Stockholm, Sweden..
    Kvarnstrom, Marika
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden..
    Grosso, Giorgia
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden..
    Rönnelid, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Padykov, Leonid
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden..
    Gunnarsson, Iva
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden..
    Silverman, Gregg J.
    NYU, Sch Med, Dept Med, Div Rheumatol, New York, NY USA..
    Svenungsson, Elisabet
    Karolinska Univ Hosp, Karolinska Inst, Dept Med, Rheumatol Unit, Stockholm, Sweden..
    Depressed serum IgM levels in SLE are restricted to defined subgroups2017Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 183, s. 304-315Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Natural IgM autoantibodies have been proposed to convey protection from autoimmune pathogenesis. Herein, we investigated the IgM responses in 396 systemic lupus erythematosus (SLE) patients, divided into subgroups based on distinct autoantibody profiles. Depressed IgM levels were more common in SLE than in matched population controls. Strikingly, an autoreactivity profile defined by IgG anti-Ro/La was associated with reduced levels of specific natural IgM targeting phosphoiylcholine (PC) antigens and malondialdehyde (MDA) modified-protein, as well as total IgM, while no differences were detected in SLE patients with an autoreactivity profile defined by anti-cardiolipin/beta(2)glycoprotein-I. We also observed an association of reduced IgM levels with the HEA-DRB1*03 allelic variant among SLE patients and controls. Associations of low IgM anti-PC with cardiovascular disease were primarily found in patients without antiphospholipid antibodies. These studies further highlight the clinical relevance of depressed IgM. Our results suggest that low IgM levels in SLE patients reflect immunological and genetic differences between SLE subgroups.

  • 6.
    Harris, Valerie M.
    et al.
    Oklahoma Medical Research Fdn, USA; University of Oklahoma, USA.
    Sharma, Rohan
    University of Oklahoma,USA; Department Vet Affairs Medical Centre, OK USA.
    Cavett, Joshua
    Oklahoma Medical Research Fdn, USA; University of Oklahoma, USA.
    Kurien, Biji T.
    Oklahoma Medical Research Fdn, USA; University of Oklahoma, USA; Department Vet Affairs Medical Centre, OK USA.
    Liu, Ke
    Cincinnati Childrens Hospital Medical Centre, USA; University of Cincinnati, USA.
    Koelsch, Kristi A.
    Oklahoma Medical Research Fdn, USA; University of Oklahoma, USA; Department Vet Affairs Medical Centre, USA.
    Rasmussen, Astrid
    Oklahoma Medical Research Fdn, USA.
    Radfar, Lida
    University of Oklahoma, USA.
    Lewis, David
    University of Oklahoma, USA.
    Stone, Donald U.
    University of Oklahoma, USA; University of Oklahoma, USA.
    Erick Kaufman, C.
    University of Oklahoma, USA.
    Li, Shibo
    University of Oklahoma, USA.
    Segal, Barbara
    University of Minnesota, USA.
    Wallace, Daniel J.
    Cedars Sinai Medical Centre, USA.
    Weisman, Michael H.
    Cedars Sinai Medical Centre, USA.
    Venuturupalli, Swamy
    Cedars Sinai Medical Centre, USA.
    Kelly, Jennifer A.
    Oklahoma Medical Research Fdn, USA.
    Alarcon-Riquelme, Marta E.
    Oklahoma Medical Research Fdn, USA; University of Granada, Spain.
    Pons-Estel, Bernardo
    Sanat Parque, Argentina.
    Jonsson, Roland
    University of Bergen, Norway; Haukeland Hospital, Norway.
    Lu, Xianglan
    University of Oklahoma, USA.
    Gottenberg, Jacques-Eric
    Strasbourg University, France.
    Anaya, Juan-Manuel
    University of Rosario, Colombia.
    Cunninghame-Graham, Deborah S.
    Kings Coll London, England.
    Huang, Andrew J. W.
    University of Minnesota, USA.
    Brennan, Michael T.
    Carolinas Medical Centre, USA.
    Hughes, Pamela
    University of Minnesota, MN USA.
    Alevizos, Ilias
    National Institute Dent and Craniofacial Research, MD USA.
    Miceli-Richard, Corinne
    University of Paris 11, France.
    Keystone, Edward C.
    Mt Sinai Hospital, Canada; University of Toronto, Canada.
    Bykerk, Vivian P.
    Hospital Special Surg, NY USA.
    Hirschfield, Gideon
    University of Birmingham, England.
    Xie, Gang
    University of Toronto, Canada.
    Ng, Wan-Fai
    Newcastle University, England.
    Nordmark, Gunnel
    Uppsala University, Sweden.
    Magnusson Bucher, Sara
    Örebro University Hospital, Sweden.
    Eriksson, Per
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Omdal, Roald
    Stavanger University Hospital, Norway.
    Rhodus, Nelson L.
    University of Minnesota, USA.
    Rischmueller, Maureen
    Queen Elizabeth Hospital, Australia; University of Adelaide, Australia.
    Rohrer, Michael
    University of Minnesota, USA.
    Wahren-Herlenius, Marie
    Karolinska Institute, Sweden.
    Witte, Torsten
    Hannover Medical Sch, Germany.
    Mariette, Xavier
    University of Paris 11, France.
    Lessard, Christopher J.
    Oklahoma Medical Research Fdn, USA.
    Harley, John B.
    Cincinnati Childrens Hospital Medical Centre, USA; University of Cincinnati, OH USA; Department Vet Affairs Medical Centre, OH USA.
    Sivils, Kathy L.
    Oklahoma Medical Research Fdn, USA; University of Oklahoma, OK 73190 USA.
    Scofield, R. Hal
    Oklahoma Medical Research Fdn, USA; University of Oklahoma, OK 73190 USA; University of Oklahoma, OK 73190 USA; Department Vet Affairs Medical Centre, OK USA.
    Klinefelters syndrome (47,XXY) is in excess among men with Sjogrens syndrome2016Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 168, s. 25-29Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Primary Sjogrens syndrome (pSS) has a strong female bias. We evaluated an X chromosome dose effect by analyzing 47,XXY (Klinefelters syndrome, 1 in 500 live male births) among subjects with pSS. 47,XXY was determined by examination of fluorescence intensity of single nucleotide polymorphisms from the X and Y chromosomes. Among 136 pSS men there were 4 with 47,XXY. This was significantly different from healthy controls (1 of 1254 had 47)0(Y, p = 0.0012 by Fishers exact test) as well men with rheumatoid arthritis (0 of 363 with 47,XXY), but not different compared to men with systemic lupus erythematosus (SLE) (4 of 136 versus 8 of 306, Fishers exact test p = NS). These results are consistent with the hypothesis that the number of X chromosomes is critical for the female bias of pSS, a property that may be shared with SLE but not RA. Published by Elsevier Inc.

  • 7. Harris, Valerie M.
    et al.
    Sharma, Rohan
    Cavett, Joshua
    Kurien, Biji T
    Liu, Ke
    Koelsch, Kristi A
    Rasmussen, Astrid
    Radfar, Lida
    Lewis, David
    Stone, Donald U
    Kaufman, C Erick
    Li, Shibo
    Segal, Barbara
    Wallace, Daniel J
    Weisman, Michael H
    Venuturupalli, Swamy
    Kelly, Jennifer A
    Alarcon-Riquelme, Marta E
    Pons-Estel, Bernardo
    Jonsson, Roland
    Lu, Xianglan
    Gottenberg, Jacques-Eric
    Anaya, Juan-Manuel
    Cunninghame-Graham, Deborah S
    Huang, Andrew J W
    Brennan, Michael T
    Hughes, Pamela
    Alevizos, Ilias
    Miceli-Richard, Corinne
    Keystone, Edward C
    Bykerk, Vivian P
    Hirschfield, Gideon
    Xie, Gang
    Ng, Wan-Fai
    Nordmark, Gunnel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Bucher, Sara Magnusson
    Eriksson, Per
    Omdal, Roald
    Rhodus, Nelson L
    Rischmueller, Maureen
    Rohrer, Michael
    Wahren-Herlenius, Marie
    Witte, Torsten
    Mariette, Xavier
    Lessard, Christopher J
    Harley, John B
    Sivils, Kathy L
    Scofield, R Hal
    Klinefelter's syndrome (47,XXY) is in excess among men with Sjögren's syndrome2016Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 168, s. 25-29Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Primary Sjögren's syndrome (pSS) has a strong female bias. We evaluated an X chromosome dose effect by analyzing 47,XXY (Klinefelter's syndrome, 1 in 500 live male births) among subjects with pSS. 47,XXY was determined by examination of fluorescence intensity of single nucleotide polymorphisms from the X and Y chromosomes. Among 136 pSS men there were 4 with 47,XXY. This was significantly different from healthy controls (1 of 1254 had 47,XXY, p=0.0012 by Fisher's exact test) as well men with rheumatoid arthritis (0 of 363 with 47,XXY), but not different compared to men with systemic lupus erythematosus (SLE) (4 of 136 versus 8 of 306, Fisher's exact test p=NS). These results are consistent with the hypothesis that the number of X chromosomes is critical for the female bias of pSS, a property that may be shared with SLE but not RA.

  • 8.
    Harris, Valerie M.
    et al.
    Oklahoma Med Res Fdn, OK 73104 USA; Univ Oklahoma, OK 73190 USA.
    Sharma, Rohan
    Univ Oklahoma, OK 73190 USA; US Dept Vet Affairs, OK USA.
    Cavett, Joshua
    Oklahoma Med Res Fdn, OK 73104 USA; Univ Oklahoma, OK 73190 USA.
    Kurien, Biji T.
    Oklahoma Med Res Fdn, OK 73104 USA; Univ Oklahoma, OK 73190 USA; US Dept Vet Affairs, OK USA.
    Liu, Ke
    Cincinnati Childrens Hosp Med Ctr, OH 45229 USA; Univ Cincinnati, OH USA.
    Koelsch, Kristi A.
    Oklahoma Med Res Fdn, OK 73104 USA; Univ Oklahoma, OK 73190 USA; US Dept Vet Affairs, OK USA.
    Rasmussen, Astrid
    Oklahoma Med Res Fdn, OK 73104 USA.
    Radfar, Lida
    Univ Oklahoma, OK 73190 USA.
    Lewis, David
    Univ Oklahoma, OK 73190 USA.
    Stone, Donald U.
    Univ Oklahoma, OK 73190 USA; Univ Oklahoma, OK 73190 USA.
    Kaufman, C. Erick
    Univ Oklahoma, OK 73190 USA.
    Li, Shibo
    Univ Oklahoma, OK 73190 USA; Univ Granada, Spain.
    Segal, Barbara
    Univ Minnesota, MN 55455 USA.
    Wallace, Daniel J.
    Cedars Sinai Med Ctr, CA 90048 USA.
    Weisman, Michael H.
    Cedars Sinai Med Ctr, CA 90048 USA.
    Venuturupalli, Swamy
    Cedars Sinai Med Ctr, CA 90048 USA.
    Kelly, Jennifer A.
    Oklahoma Med Res Fdn, OK 73104 USA.
    Alarcon-Riquelme, Marta E.
    Oklahoma Med Res Fdn, OK 73104 USA.
    Pons-Estel, Bernardo
    Sanatorio Parque, Argentina.
    Jonsson, Roland
    Univ Bergen, Norway; Haukeland Hosp, Norway.
    Lu, Xianglan
    Univ Oklahoma, OK 73190 USA; Univ Granada, Spain.
    Gottenberg, Jacques-Eric
    Strasbourg Univ, France.
    Anaya, Juan-Manuel
    Univ Rosario, Colombia.
    Cunninghame-Graham, Deborah S.
    Kings Coll London, England; Karolinska Inst, Sweden; Kings Coll London, England.
    Huang, Andrew J. W.
    Univ Minnesota, MN USA.
    Brennan, Michael T.
    Carolinas Med Ctr, NC 28232 USA.
    Hughes, Pamela
    Univ Minnesota, MN USA.
    Alevizos, Ilias
    Natl Inst Dent and Craniofacial Res, MD USA.
    Miceli-Richard, Corinne
    Univ Paris Sud, France.
    Keystone, Edward C.
    Mt Sinai Hosp, Canada; Univ Toronto, Canada.
    Bykerk, Vivian P.
    Hosp Special Surg, NY 10021 USA.
    Hirschfield, Gideon
    Univ Birmingham, England.
    Xie, Gang
    Samuel Lunenfeld Res Inst, Canada; Toronto Gen Res Inst, Canada; Univ Toronto, Canada; Univ Toronto, Canada; Univ Toronto, Canada.
    Siminovitch, Katherine A.
    Samuel Lunenfeld Res Inst, Canada; Toronto Gen Res Inst, Canada; Univ Toronto, Canada; Univ Toronto, Canada; Univ Toronto, Canada.
    Ng, Wan-Fai
    Newcastle Univ, England; Newcastle Univ, England.
    Nordmark, Gunnel
    Uppsala Univ, Sweden; Uppsala Univ, Sweden.
    Bucher, Sara Magnusson
    Oklahoma Med Res Fdn, OK 73104 USA; Univ Oklahoma, OK 73190 USA.
    Eriksson, Per
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Omdal, Roald
    Stavanger Univ Hosp, Norway.
    Rhodus, Nelson L.
    Univ Minnesota, MN 55455 USA.
    Rischmueller, Maureen
    Queen Elizabeth Hosp, Australia; Univ Adelaide, Australia.
    Rohrer, Michael
    Univ Minnesota, MN USA.
    Wahren-Herlenius, Marie
    Karolinska Inst, Sweden.
    Witte, Torsten
    Hannover Med Sch, Germany.
    Mariette, Xavier
    Univ Paris Sud, France.
    Lessard, Christopher J.
    Oklahoma Med Res Fdn, OK 73104 USA.
    Harley, John B.
    Cincinnati Childrens Hosp Med Ctr, OH 45229 USA; Univ Cincinnati, OH USA; US Dept Vet Affairs, OH USA.
    Sivils, Kathy L.
    Oklahoma Med Res Fdn, OK 73104 USA; Univ Oklahoma, OK 73190 USA.
    Scofield, R. Hal
    Oklahoma Med Res Fdn, OK 73104 USA; Univ Oklahoma, OK 73190 USA; Univ Oklahoma, OK 73190 USA; US Dept Vet Affairs, OK USA.
    Correction: Klinefelters syndrome (47,XXY) is in excess among men with Sjogrens syndrome (vol 168, pg 25, 2016)2018Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 187, s. 137-138Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    n/a

  • 9. Hjorth, Maria
    et al.
    Axelsson, Stina
    Rydén, Anna
    Faresjö, Maria
    Högskolan i Jönköping, Hälsohögskolan, HHJ. Biomedicinsk plattform. Högskolan i Jönköping, Hälsohögskolan, HHJ, Avd. för naturvetenskap och biomedicin.
    Ludvigsson, Johnny
    Casas, Rosaura
    GAD-alum treatment induces GAD65-specific CD4+CD25highFOXP3+ cells in type 1 diabetic patients.2011Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 138, nr 1, s. 117-126Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Type 1 diabetes results from autoimmune destruction of insulin producing pancreatic β-cells. We have shown that treatment with alum-formulated glutamic acid decarboxylase 65 (GAD-alum) preserved residual insulin secretion and induced antigen-specific responses in children with recent onset type 1 diabetes. The aim of this study was to further investigate the immunomodulatory effect of GAD-alum, focusing on CD4+CD25high cells and their association to cytokine secretion. Samples obtained 21 and 30 months after the initial injection of GAD-alum or placebo were included in the present study. GAD65-stimulation enhanced the percentage of CD4+CD25highFOXP3+ cells, but reduced the percentage of CD4+CD25+ cells, in samples from the GAD-alum treated group. Further, the GAD65-induced secretion of IL-5, -10, and -13 correlated with the expression of CD4+CD25highFOXP3+ cells, but inversely with CD4+CD25+ cells. These new data suggest that GAD-alum treatment induced GAD65-specific T cells with regulatory features.

  • 10.
    Imgenberg-Kreuz, Juliana
    et al.
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi.
    Sandling, Johanna K.
    Uppsala universitet, Science for Life Laboratory, SciLifeLab. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi.
    Nordmark, Gunnel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Reumatologi. Uppsala universitet, Science for Life Laboratory, SciLifeLab.
    Epigenetic alterations in primary Sjogren's syndrome: an overview2018Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 196, s. 12-20Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Primary Sjogren's syndrome (pSS) is a chronic autoimmune rheumatic disease characterized by inflammation of exocrine glands, mainly salivary and lacrimal glands. In addition, pSS may affect multiple other organs resulting in systemic manifestations. Although the precise etiology of pSS remains elusive, pSS is considered to be a multi factorial disease, where underlying genetic predisposition, environmental factors and epigenetic mechanisms contribute to disease development. Epigenetic mechanisms, such as DNA methylation, histone modifications and non-coding RNAs, may constitute a dynamic link between genome, environment and phenotypic manifestation by their modulating effects on gene expression. A growing body of studies reporting altered epigenetic landscapes in pSS suggests that epigenetic mechanisms play a role in the pathogenesis of pSS, and the reversible nature of epigenetic modifications suggests therapeutic strategies targeting epigenetic dysregulation in pSS. This article reviews our current understanding of epigenetic mechanisms in pSS and discusses implications for novel diagnostic and therapeutic approaches.

  • 11. Janzi, Magdalena
    et al.
    Kull, Inger
    Sjöberg, Ronald
    KTH, Skolan för bioteknologi (BIO), Proteomik.
    Wan, Jinghong
    KTH, Skolan för bioteknologi (BIO), Proteomik.
    Melen, Erik
    Bayat, Narges
    Ostblom, Eva
    Pan-Hammarstrom, Qiang
    Nilsson, Peter
    KTH, Skolan för bioteknologi (BIO), Proteomik.
    Hammarstrom, Lennart
    Selective IgA deficiency in early life: Association to infections and allergic diseases during childhood2009Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 133, nr 1, s. 78-85Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Selective IgA deficiency in early life is quite common in Caucasian populations, but it is unclear whether it increases the risk of infections and allergic diseases during childhood. Serum IgA levels were measured in 2423 children at 4 years of age in a Swedish population based birth cohort (BAMSE). Parental questionnaires were repeatedly sent out during the child's first 8 years of life, collecting information about infections and allergic diseases. 14 children (1:173) were found to be IgA deficient at 4 years of age. These children had an increased risk of pseudocroup at year 1 (p<0.01) and food hypersensitivity at year 4 (p<0.05) as compared to IgA sufficient children. No increased risk was observed in the partial IgA deficiency group. The findings suggest that selective IgA deficiency may increase the risk of parentally reported pseudocroup and food hypersensitivity during early childhood.

  • 12.
    Lindblom, Rickard
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Thoraxkirurgi.
    Aeinehband, Shahin
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
    Ström, Mikael
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
    Al Nimer, Faiez
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
    Sandholm, Kerstin
    Linnaeus Univ, Linnaeus Ctr Biomat Chem, S-39182 Kalmar, Sweden.
    Khademi, Mohsen
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Piehl, Fredrik
    Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
    Ekdahl Nilsson, Kristina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Complement Receptor 2 is increased in cerebrospinal fluid of multiple sclerosis patients and regulates C3 function2016Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 166, s. 89-95Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Besides its vital role in immunity, the complement system also contributes to the shaping of the synaptic circuitry of the brain. We recently described that soluble Complement Receptor 2 (sCR2) is part of the nerve injury response in rodents. We here study CR2 in context of multiple sclerosis (MS) and explore the molecular effects of CR2 on 0 activation. Significant increases in sCR2 levels were evident in cerebrospinal fluid (CSF) from both patients with relapsing remitting MS (n = 33; 6.2 ng/mL) and secondary-progressive MS (n = 9; 7.0 ng/mL) as compared to controls (n = 18; 4.1 ng/mL). Furthermore, CSF sCR2 levels correlated significantly both with CSF C3 and C1q as well as to a disease severity measure. In vitro, sCR2 inhibited the cleavage and down regulation of Cab to iC3b, suggesting that it exerts a modulatory role in complement activation downstream of C3. These results propose a novel function for CR2/sCR2 in human neuroinflammatory conditions.

  • 13.
    Lindblom, Rickard P. F.
    et al.
    Karolinska Institutet;Uppsala University.
    Aeinehband, Shainn
    Karolinska Institutet.
    Ström, Mikael
    Karolinska Institutet.
    Al Nimer, Faiez
    Karolinska Institutet.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB).
    Khademi, Mohsen
    Karolinska Institutet.
    Nilsson, Bo
    Uppsala University.
    Piehl, Fredrik
    Karolinska Institutet.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Complement receptor 2 is increased in cerebrospinal fluid of multiple sclerosis patients and regulates C3 function2016Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 166, s. 89-95Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Besides its vital role in immunity, the complement system also contributes to the shaping of the synaptic circuitry of the brain. We recently described that soluble Complement Receptor 2 (sCR2) is part of the nerve injury response in rodents. We here study CR2 in context of multiple sclerosis (MS) and explore the molecular effects of CR2 on C3 activation.

    Significant increases in sCR2 levels were evident in cerebrospinal fluid (CSF) from both patients with relapsing-remitting MS (n = 33; 6.2 ng/mL) and secondary-progressive MS (n = 9; 7.0 ng/mL) as compared to controls (n = 18; 4.1 ng/mL). Furthermore, CSF sCR2 levels correlated significantly both with CSF C3 and C1q as well as to a disease severity measure. In vitro, sCR2 inhibited the cleavage and down regulation of C3b to iC3b, suggesting that it exerts a modulatory role in complement activation downstream of C3.

    These results propose a novel function for CR2/sCR2 in human neuroinflammatory conditions.

  • 14. Lindblom, Rickard PF
    et al.
    Aeinehband, Shahen
    Ström, Mikael
    Al Nimer, Faiez
    Sandholm, Kerstin
    Khademi, Mohsen
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Piehl, Fredrik
    Ekdahl, Kristina N
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Complement receptor 2 is increased in cerebrospinal fluid of multiple sclerosis patients and regulates C3 functionIngår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035Artikel i tidskrift (Refereegranskat)
  • 15. Lourda, Magda
    et al.
    Olsson-Akefeldt, Selma
    Gavhed, Desiree
    Bjornfot, Sofia
    Clausen, Niels
    Hjalmars, Ulf
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Sabel, Magnus
    Tazi, Abdellatif
    Arico, Maurizio
    Delprat, Christine
    Henter, Jan-Inge
    Svensson, Mattias
    Detection of IL-17A-producing peripheral blood monocytes in Langerhans cell histiocytosis patients2014Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 153, nr 1, s. 112-122Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Langerhans cell histiocytosis (LCH) is a rare disease of unknown cause with manifestations ranging from isolated granulomatous lesions to life-threatening multi-system organ involvement. This disorder is further characterized by infiltration of immune cells in affected tissues and an association with interleukin (IL)-17A has been reported. Here, we investigated the presence of IL-17A-producing cells among peripheral blood mononuclear cells isolated from LCH patients and observed a high percentage of IL-17A(+) monocytes in peripheral blood of LCH patients compared to controls. The IL-17A(+) monocytes were also positive for the transcription factor retinoic acid orphan receptor (ROR) gamma t and showed increased mRNA levels for both IL-17A and ROR gamma t. Notably, IL-17A was produced by all monocyte subsets and the expression level was positively associated with LCH disease activity. These data support a role for monocytes in the pathogenesis of LCH. Future therapeutic approaches may consider identification of patients who may benefit from IL-17A-targeted interventions.

  • 16.
    Lundin, Karin E.
    et al.
    Karolinska Inst, Clin Res Ctr, Dept Lab Med, Karolinska Univ Hosp, S-14186 Huddinge, Sweden..
    Hamasy, Abdulrahman
    Karolinska Inst, Clin Res Ctr, Dept Lab Med, Karolinska Univ Hosp, S-14186 Huddinge, Sweden..
    Backe, Paul Hoff
    Natl Hosp Norway, Oslo Univ Hosp, Clin Diagnost & Intervent, Dept Microbiol, N-0424 Oslo, Norway.;Univ Oslo, Inst Clin Med, Dept Med Biochem, N-0424 Oslo, Norway..
    Moens, Lotte N.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi.
    Falk-Sörqvist, Elin
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg.
    Elgstoen, Katja B.
    Univ Oslo, Inst Clin Med, Dept Med Biochem, N-0424 Oslo, Norway..
    Morkrid, Lars
    Univ Oslo, Inst Clin Med, Dept Med Biochem, N-0424 Oslo, Norway..
    Bjoras, Magnar
    Natl Hosp Norway, Oslo Univ Hosp, Clin Diagnost & Intervent, Dept Microbiol, N-0424 Oslo, Norway.;NTNU, Inst Canc Res & Mol Med, N-7491 Trondheim, Norway..
    Granert, Carl
    Karolinska Univ Hosp, Clin Immunol Sect, Immunodeficiency Unit, S-14186 Stockholm, Sweden..
    Norlin, Anna-Carin
    Karolinska Univ Hosp, Clin Immunol Sect, Immunodeficiency Unit, S-14186 Stockholm, Sweden.;Karolinska Univ Hosp, Karolinska Univ Lab, Clin Immunol & Transfus Med, S-14186 Huddinge, Sweden..
    Nilsson, Mats
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Molekylära verktyg. Stockholm Univ, Dept Biochem & Biophys, Sci Life Lab, S-17121 Stockholm, Sweden..
    Christensson, Birger
    Karolinska Inst, Div Pathol, Dept Lab Med, S-14186 Stockholm, Sweden..
    Stenmark, Stephan
    Umea Univ, Dept Clin Microbiol, S-90187 Umea, Sweden..
    Smith, C. I. Edvard
    Karolinska Inst, Clin Res Ctr, Dept Lab Med, Karolinska Univ Hosp, S-14186 Huddinge, Sweden.;Karolinska Univ Hosp, Clin Immunol Sect, Immunodeficiency Unit, S-14186 Stockholm, Sweden..
    Susceptibility to infections, without concomitant hyper-IgE, reported in 1976, is caused by hypomorphic mutation in the phosphoglucomutase 3 (PGM3) gene2015Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 161, nr 2, s. 366-372Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Phosphoglucomutase 3 (PGM3) is an enzyme converting N-acetyl-glucosamine-6-phosphate to N-acetylglucosamine-l-phosphate, a precursor important for glycosylation. Mutations in the PGM3 gene have recently been identified as the cause of novel primary immunodeficiency with a hyper-IgE like syndrome. Here we report the occurrence of a homozygous mutation in the PGM3 gene in a family with immunodeficient children, described already in 1976. DNA from two of the immunodeficient siblings was sequenced and shown to encode the same homozygous missense mutation, causing a destabilized protein with reduced enzymatic capacity. Affected individuals were highly prone to infections, but lack the developmental defects in the nervous and skeletal systems, reported in other families. Moreover, normal IgE levels were found. Thus, belonging to the expanding group of congenital glycosylation defects, PGM3 deficiency is characterized by immunodeficiency, with or without increased IgE levels, and with variable forms of developmental defects affecting other organ systems.

  • 17. Lundin, Karin E.
    et al.
    Hamasy, Abdulrahman
    Backe, Paul Hoff
    Moens, Lotte N.
    Falk-Sörqvist, Elin
    Elgstøen, Katja B.
    Mørkrid, Lars
    Bjørås, Magnar
    Granert, Carl
    Norlin, Anna-Carin
    Nilsson, Mats
    Stockholms universitet, Science for Life Laboratory (SciLifeLab). Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för biokemi och biofysik. Uppsala University, Sweden.
    Christensson, Birger
    Stenmark, Stephan
    Smith, C. I. Edvard
    Susceptibility to infections, without concomitant hyper-IgE, reported in 1976, is caused by hypomorphic mutation in the phosphoglucomutase 3 (PGM3) gene2015Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 161, nr 2, s. 366-372Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Phosphoglucomutase 3 (PGM3) is an enzyme converting N-acetyl-glucosamine-6-phosphate to N-acetylglucosamine-l-phosphate, a precursor important for glycosylation. Mutations in the PGM3 gene have recently been identified as the cause of novel primary immunodeficiency with a hyper-IgE like syndrome. Here we report the occurrence of a homozygous mutation in the PGM3 gene in a family with immunodeficient children, described already in 1976. DNA from two of the immunodeficient siblings was sequenced and shown to encode the same homozygous missense mutation, causing a destabilized protein with reduced enzymatic capacity. Affected individuals were highly prone to infections, but lack the developmental defects in the nervous and skeletal systems, reported in other families. Moreover, normal IgE levels were found. Thus, belonging to the expanding group of congenital glycosylation defects, PGM3 deficiency is characterized by immunodeficiency, with or without increased IgE levels, and with variable forms of developmental defects affecting other organ systems.

  • 18. Lundin, Karin E
    et al.
    Hamasy, Abdulrahman
    Backe, Paul Hoff
    Moens, Lotte N
    Falk-Sörqvist, Elin
    Elgstøen, Katja B
    Mørkrid, Lars
    Bjørås, Magnar
    Granert, Carl
    Norlin, Anna-Carin
    Nilsson, Mats
    Christensson, Birger
    Stenmark, Stephan
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi.
    Smith, C I Edvard
    Susceptibility to infections, without concomitant hyper-IgE, reported in 1976, is caused by hypomorphic mutation in the phosphoglucomutase 3 (PGM3) gene2015Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 161, nr 2, s. 366-372Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Phosphoglucomutase 3 (PGM3) is an enzyme converting N-acetyl-glucosamine-6-phosphate to N-acetylglucosamine-l-phosphate, a precursor important for glycosylation. Mutations in the PGM3 gene have recently been identified as the cause of novel primary immunodeficiency with a hyper-IgE like syndrome. Here we report the occurrence of a homozygous mutation in the PGM3 gene in a family with immunodeficient children, described already in 1976. DNA from two of the immunodeficient siblings was sequenced and shown to encode the same homozygous missense mutation, causing a destabilized protein with reduced enzymatic capacity. Affected individuals were highly prone to infections, but lack the developmental defects in the nervous and skeletal systems, reported in other families. Moreover, normal IgE levels were found. Thus, belonging to the expanding group of congenital glycosylation defects, PGM3 deficiency is characterized by immunodeficiency, with or without increased IgE levels, and with variable forms of developmental defects affecting other organ systems.

  • 19.
    Magnusson, Sofia
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Andrén, Maria
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Nilsson, Kajsa E
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Sondermann, Peter
    Jacob, Uwe
    Kleinau, Sandra
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi.
    Amelioration of collagen-induced arthritis by human recombinant soluble FcγRIIb2008Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 127, nr 2, s. 225-233Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Immune complex (IC) binding to Fc gamma receptors (FcγRs) is central for inflammatory reactions seen in autoimmune diseases. Consequently, a therapeutic agent with a possibility to interfere with binding of pathogenic IC to FcγRs would be valuable in autoimmune disorders such as rheumatoid arthritis (RA). Here we have explored the therapeutic effect of a recombinant solublehuman FcγRIIb (sFcγRIIb) protein in collagen-induced arthritis (CIA). In vitro studies of the sFcγRIIb demonstrated binding to mouse IgG, suggesting that sFcγRIIb can absorb pathogenic IgG anticollagen type II (CII) IC in vivo. Hence, administration of sFcγRIIb significantly reduced CIA severity compared to control treated mice. The sFcγRIIb treated mice had significantly less IgG anti-CII antibodies in serum and lowermRNA levels of inflammatory cytokines compared to controlmice. In conclusion, sFcγRIIb treatment ameliorates CIA by reducing IC-stimulated inflammation and joint swelling. This suggests that recombinant sFcγRIIb may be useful as therapeutic agent in RA.

  • 20.
    Marits, Per
    et al.
    Karolinska Institutet, Sweden.
    Wikstrom, Ann-Charlotte
    Karolinska Institutet, Sweden.
    Popadic, Dusan
    University of Belgrade, Serbia.
    Winqvist, Ola
    Karolinska institutet, Sweden.
    Thunberg, Sarah
    Karolinska Institutet, Sweden.
    Evaluation of T and B lymphocyte function in clinical practice using a flow cytometry based proliferation assay2014Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 153, nr 2, s. 332-342Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The golden standard for functional evaluation of immunodeficiencies is the incorporation of [H-3]-thymidine in a proliferation assay stimulated with mitogens. Recently developed whole blood proliferation assays have the advantage of parallel lymphocyte lineage analysis and in addition provide a non-radioactive alternative. Here we evaluate the Flow-cytometric Assay for Specific Cell-mediated Immune-response in Activated whole blood (FASCIA) in a comparison with [H-3]-thymidine incorporation in four patients with severe combined immunodeficiency. The threshold for the mininium number of lymphocytes required for reliable responses in FASCIA is determined together with reference values from 100 healthy donors when stimulated with mitogens as well as antigen specific stimuli. Finally, responses against PWM and SEA + SEB stimuli are conducted with clinically relevant immunomodulatory compounds. We conclude that FASCIA is a rapid, stable and sensitive functional whole blood assay that requires small amounts of whole blood that can be used for reliable assessment of lymphocyte reactivity in patients. (C) 2014 Elsevier Inc. All rights reserved.

  • 21. Oftedal, Bergithe E
    et al.
    Wolff, Anette S Bøe
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Bratland, Eirik
    Kämpe, Olle
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Perheentupa, Jaakko
    Myhre, Anne Grethe
    Meager, Anthony
    Purushothaman, Radhika
    Ten, Svetlana
    Husebye, Eystein S
    Radioimmunoassay for autoantibodies against interferon omega; its use in the diagnosis of autoimmune polyendocrine syndrome type I2008Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 129, nr 1, s. 163-9Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Patients with the autoimmune polyendocrine syndrome I (APS I) have high titers of neutralizing IgG autoantibodies against type I interferons (IFNs), in particular IFN-omega. Until now, the most specific assay has been the antiviral interferon neutralizing assay (AVINA), which has the drawbacks of requiring a cytolytic virus, being cumbersome and difficult to standardise. We have developed a fast and reliable immunoassay based on radiolabelled IFN-omega for quantifying anti-IFN-omega antibodies. Sera from 48 APS I patients were analysed together with those from 5 control groups. All sera from APS I patients were positive for anti-IFN-omega, while, except one serum, all sera from the controls were negative. This method has the advantage over bioassays that it is readily adapted to high throughput. It provides an alternative, sensitive and specific diagnostic test for APS I, and an ideal screening tool to precede mutational analyses of the AIRE gene in suspected APS I cases.

  • 22.
    Pihl, Mikael
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Barcenilla, Hugo
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Medicinska fakulteten.
    Axelsson Chéramy, Stina
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Medicinska fakulteten.
    Chéramy, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Medicinska fakulteten.
    Åkerman, Linda
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten.
    Johansson, Ingela
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten.
    Ludvigsson, Johnny
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Casas, Rosaura
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för barns och kvinnors hälsa. Linköpings universitet, Medicinska fakulteten.
    GAD-specific T cells are induced by GAD-alum treatment in Type-1 diabetes patients2017Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 176, s. 114-121Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Administration of Glutamic Acid Decarboxylase (GAD)(65) formulated in aluminium hydroxide preserved insulin secretion in a phase II trial in recent onset Type 1 Diabetes. A subsequent European phase III trial was closed at 15 months after failing to reach primary endpoint, but the majority of the Swedish patients completed the 21 months follow-up. We studied the frequencies and phenotype of T cells, suppressive capacity of Tregs, GAD(65)-induced proliferation, and frequencies of T cells with a GAD(65)-specific TCR in Swedes participating in the trial. Stimulation with GAD(65) induced activated T cells and also cells with a suppressive phenotype. Activated GAD(65)-specific effector T cells were detected by tetramer staining while the frequency of GAD(65)-specific Treg was not affected by the treatment. Additional doses of GAD-alum increased frequencies of CD25(+)CD127(+), but had no effect on CD25(hi)CD127(lo). Our findings indicate that GAD-alum treatment primarily induced activated T cells. GAD(65)-specific cells were mainly of activated phenotype. (C) 2017 Elsevier Inc. All rights reserved.

  • 23.
    Prokopec, Kajsa
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Molekylär immunologi.
    Rhodiner, Mia
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Molekylär immunologi.
    Matt, Peter
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Lindqvist, Ulla
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper.
    Kleinau, Sandra
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för cell- och molekylärbiologi, Molekylär immunologi.
    Down regulation of Fc and complement receptors on B cells in rheumatoid arthritis2010Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 137, nr 3, s. 322-329Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    B cell tolerance is regulated by receptors that modulate B cell receptor signaling, such as Fc gamma receptor IIb (FcγRIIb; CD32b) and complement receptors (CR) 1 and 2. Deficiency in these receptors may contribute to autoimmunity. To address this we have investigated the receptor expression in healthy individuals in comparison with rheumatoid arthritis (RA) patients. In healthy subjects we found that women had overall lower Fcgamma;RIIb expression on B cells than men that significantly decreased with age. RA patients had fewer FcγRIIb, CR1 and CR2 positive B cells and decreased receptor expressions compared to healthy subjects. Further, the RA B cells displayed a significantly increased proliferative response when cultured with interleukin-2 in vitro. In summary, the dysregulated B cells in RA are associated with lower FcγRIIb, CR1 and CR2 levels. The reduced FcγRIIb expression on B cells in women may influence the increased frequency of autoimmunity in women.

  • 24.
    Reis, Edimara S.
    et al.
    Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
    Berger, Nadja
    Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
    Wang, Xin
    Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
    Koutsogiannaki, Sophia
    Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
    Doot, Robert K.
    Univ Penn, Perelman Sch Med, Dept Radiol, Philadelphia, PA 19104 USA.
    Gumas, Justin T.
    Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
    Foukas, Periklis G.
    Univ Athens, Attikon Univ Hosp, Dept Pathol 2, Athens, Greece.
    Resuello, Ranillo R. G.
    Simian Conservat Breeding & Res Ctr SICONBREC, Makati, Philippines.
    Tuplano, Joel V.
    Simian Conservat Breeding & Res Ctr SICONBREC, Makati, Philippines.
    Kukis, David
    Univ Calif Davis, Ctr Mol & Genom Imaging, Davis, CA 95616 USA.
    Tarantal, Alice F.
    Univ Calif Davis, Sch Med, Dept Pediat, Davis, CA 95616 USA;Univ Calif Davis, Sch Med, Dept Cell Biol & Human Anat, Davis, CA 95616 USA;Univ Calif Davis, Calif Natl Primate Res Ctr, Davis, CA 95616 USA.
    Young, Anthony J.
    Univ Penn, Perelman Sch Med, Dept Radiol, Philadelphia, PA 19104 USA.
    Kajikawa, Tetsuhiro
    Univ Penn, Sch Dent Med, Dept Microbiol, Philadelphia, PA 19104 USA.
    Soulika, Athena M.
    Univ Calif Davis, Dept Dermatol, Davis, CA 95616 USA.
    Mastellos, Dimitrios C.
    Natl Ctr Sci Res Demokritos, Athens, Greece.
    Yancopoulou, Despina
    Amyndas Pharmaceut, Glifadha, Greece.
    Biglarnia, Ali-Reza
    Lund Univ, Skane Univ Hosp, Dept Transplantat, Lund, Sweden.
    Huber-Lang, Markus
    Univ Hosp Ulm, Inst Clin & Expt Trauma Immunol, Ulm, Germany.
    Hajishengallis, George
    Univ Penn, Sch Dent Med, Dept Microbiol, Philadelphia, PA 19104 USA.
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Lambris, John D.
    Univ Penn, Perelman Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA.
    Safety profile after prolonged C3 inhibition2018Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 197, s. 96-106Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The central component of the complement cascade, C3, is involved in various biological functions, including opsonization of foreign bodies, clearance of waste material, activation of immune cells, and triggering of pathways controlling development. Given its broad role in immune responses, particularly in phagocytosis and the clearance of microbes, a deficiency in complement C3 in humans is often associated with multiple bacterial infections. Interestingly, an increased susceptibility to infections appears to occur mainly in the first two years of life and then wanes throughout adulthood. In view of the well-established connection between C3 deficiency and infections, therapeutic inhibition of complement at the level of C3 is often considered with caution or disregarded. We therefore set out to investigate the immune and biochemical profile of non-human primates under prolonged treatment with the C3 inhibitor compstatin (Cp40 analog). Cynomolgus monkeys were dosed subcutaneously with Cp40, resulting in systemic inhibition of C3, for 1 week, 2 weeks, or 3 months. Plasma concentrations of both C3 and Cp40 were measured periodically and complete saturation of plasma C3 was confirmed. No differences in hematological, biochemical, or immunological parameters were identified in the blood or tissues of animals treated with Cp40 when compared to those injected with vehicle alone. Further, skin wounds showed no signs of infection in those treated with Cp40. In fact, Cp40 treatment was associated with a trend toward accelerated wound healing when compared with the control group. In addition, a biodistribution study in a rhesus monkey indicated that the distribution of Cp40 in the body is associated with the presence of C3, concentrating in organs that accumulate blood and produce C3. Overall, our data suggest that systemic C3 inhibition in healthy adult non-human primates is not associated with a weakened immune system or susceptibility to infections.

  • 25.
    Segelmark, Mårten
    Universitetssjukhuset i Lund.
    Natural anti-GBM antibodies from normal human sera recognize alpha3 (IV) NC1 restrictively and recognize the same epitopes as anti-GBM antibodies from patients with anti-GBM disease.2007Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. Aug, nr 124(2), s. 207-12Artikel i tidskrift (Refereegranskat)
  • 26.
    Ullenhag, G
    et al.
    Radiumhemmet, CancerCentreKarolinska, Karolinska Hospital, Stockholm, Sweden. Department of Oncology, University Hospital, Uppsala, Sweden.
    Bird, C
    Division of Immunobiology, National Institute for Biological Standards and Control, Potters Bar, Herts, United Kingdom.
    Ragnhammar, P
    Radiumhemmet, CancerCentreKarolinska, Karolinska Hospital, Stockholm, Sweden. Department of Oncology, Radiumhemmet, Karolinska Hospital, Stockholm, Sweden.
    Frödin, J E
    Radiumhemmet, CancerCentreKarolinska, Karolinska Hospital, Stockholm, Sweden. Department of Oncology, Radiumhemmet, Karolinska Hospital, Stockholm, Sweden.
    Strigård, Karin
    Department of Surgery, Huddinge University Hospital, Stockholm, Sweden.
    Olsterborg, A
    Radiumhemmet, CancerCentreKarolinska, Karolinska Hospital, Stockholm, Sweden. Department of Oncology, Radiumhemmet, Karolinska Hospital, Stockholm, Sweden.
    Thorpe, R
    Division of Immunobiology, National Institute for Biological Standards and Control, Potters Bar, Herts, United Kingdom.
    Mellstedt, H
    Department of Oncology, Radiumhemmet, Karolinska Hospital, Stockholm, Sweden. Radiumhemmet, Department of Hematology, Karolinska Hospital, Stockholm, Sweden. Radiumhemmet, CancerCentreKarolinska, Karolinska Hospital, Stockholm, Sweden.
    Wadhwa, M
    Division of Immunobiology, National Institute for Biological Standards and Control, Potters Bar, Herts, United Kingdom.
    Incidence of GM-CSF antibodies in cancer patients receiving GM-CSF for immunostimulation.2001Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 99, nr 1, s. 65-74Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We have assessed the immunogenicity profile of GM-CSF in patients with either colorectal carcinoma (CRC) at different stages of disease or with multiple myeloma who were given recombinant human GM-CSF (Escherichia coli-derived) combination therapy. Metastatic CRC patients received a colon carcinoma-reactive antibody and high doses of GM-CSF (425--500 microg/day for 10 days), while other CRC patients and those with myeloma received low doses of GM-CSF (75--80 microg/day for 4 days) as an adjuvant along with appropriate tumor antigens. We found that 55% of the patients (11/20) given high doses of GM-CSF developed GM-CSF-reactive antibodies in comparison with an incidence of only 16% (4/25) in patients given low doses of GM-CSF. None of the patients developed neutralizing antibodies and so the biological effects of GM-CSF were not compromised. A majority of patients (80%) (36/45) also developed antibodies to E. coli proteins that were present as trace contaminants in the GM-CSF product. Treatment with recombinant GM-CSF products, therefore, may induce antibodies against this cytokine depending on the regimen and the amounts used. In this study, multiple immunizations with low doses of GM-CSF was associated with a low incidence of GM-CSF antibodies, which did not neutralize the effect of the cytokine. This therapeutic strategy was effective in inducing adjuvant-type effects and needs to be explored in further clinical trials with this cytokine.

  • 27. Zhu, Bing
    et al.
    Trikudanathan, Subbulaxmi
    Zozulya, Alla L.
    Sandoval-Garcia, Carolina
    Kennedy, Jennifer K.
    Atochina, Olga
    Norberg, Thomas
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Fysikalisk-organisk kemi.
    Castagner, Bastien
    Seeberger, Peter
    Fabry, Zsuzsa
    Harn, Donald
    Khoury, Samia J.
    Guleria, Indira
    Immune modulation by Lacto-N-fucopentaose III in experimental autoimmune encephalomyelitis2012Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 142, nr 3, s. 351-361Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Parasitic infections frequently lead to immune deviation or suppression. However, the application of specific parasitic molecules in regulating autoimmune responses remains to be explored. Here we report on the immune modulatory function of Lacto-N-fucopentaose III (LNFPIII), a schistosome glycan, in an animal model for multiple sclerosis. We found that LNFPIII treatment significantly reduced the severity of experimental autoimmune encephalomyelitis (EAE) and CNS inflammation, and skewed peripheral immune response to a Th2 dominant profile. Inflammatory monocytes (IMCs) purified from LNFPIII-treated mice had increased expression of nitric oxide synthase 2, and mediated T cell suppression. LNFPIII treatment also significantly increased mRNA expression of arginase-1, aldehyde dehydrogenase 1 subfamily A2, indoleamine 2,3-dioxygenase and heme oxygenase 1 in splenic IMCs. Furthermore, LNFPIII treatment significantly reduced trafficking of dendritic cells across brain endothelium in vitro. In summary, our study demonstrates that LNFPIII glycan treatment suppresses EAE by modulating both innate and T cell immune response.

  • 28. Zhu, Bing
    et al.
    Trikudanathan, Subbulaxmi
    Zozulya, Alla L
    Sandoval-Garcia, Carolina
    Kennedy, Jennifer K
    Atochina, Olga
    Norberg, Thomas
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Fysikalisk-organisk kemi.
    Castagner, Bastien
    Seeberger, Peter
    Fabry, Zsuzsa
    Harn, Donald
    Khoury, Samia J
    Guleria, Indira
    Immune modulation by Lacto-N-fucopentaose III in experimental autoimmune encephalomyelitis2012Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 142, nr 3, s. 351-361Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Parasitic infections frequently lead to immune deviation or suppression. However, the application of specific parasitic molecules in regulating autoimmune responses remains to be explored. Here we report on the immune modulatory function of Lacto-N-fucopentaose III (LNFPIII), a schistosome glycan, in an animal model for multiple sclerosis. We found that LNFPIII treatment significantly reduced the severity of experimental autoimmune encephalomyelitis (EAE) and CNS inflammation, and skewed peripheral immune response to a Th2 dominant profile. Inflammatory monocytes (IMCs) purified from LNFPIII-treated mice had increased expression of nitric oxide synthase 2, and mediated T cell suppression. LNFPIII treatment also significantly increasedmRNA expression of arginase-1, aldehyde dehydrogenase 1 subfamily A2, indoleamine 2,3-dioxygenase and heme oxygenase 1 in splenic IMCs. Furthermore, LNFPIII treatment significantly reduced trafficking of dendritic cells across brain endothelium in vitro

    . In summary, our study demonstrates that LNFPIII glycan treatment suppresses EAE by modulating both innate and T cell immune response.

  • 29. Zirakzadeh, A Ali
    et al.
    Kinn, Johan
    Krantz, David
    Rosenblatt, Robert
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi. Department of Urology, Stockholm South General Hospital, Karolinska Institutet, Stockholm, Sweden.
    Winerdal, Malin E
    Hu, Jin
    Hartana, Ciputra Adijaya
    Lundgren, Christian
    Bergman, Emma Ahlén
    Johansson, Markus
    Holmström, Benny
    Hansson, Johan
    Sidikii, Alexander
    Vasko, Janos
    Umeå universitet, Medicinska fakulteten, Institutionen för medicinsk biovetenskap, Patologi.
    Marits, Per
    Sherif, Amir
    Umeå universitet, Medicinska fakulteten, Institutionen för kirurgisk och perioperativ vetenskap, Urologi och andrologi.
    Winqvist, Ola
    Doxorubicin enhances the capacity of B cells to activate T cells in urothelial urinary bladder cancer2017Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 176, s. 63-70Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cancer is currently treated by a combination of therapies, including chemotherapy which is believed to suppress the immune system. Combination of immunotherapy and chemotherapy correlates with improved survival but needs careful planning in order to achieve a synergistic effect. In this study, we have demonstrated that doxorubicin treatment of B cells resulted in increased expression of CD86 and concordantly increased CD4(+) T cell activation in the presence of superantigen, an effect that was inhibited by the addition of a CD86 blocking antibody. Furthermore, doxorubicin resulted in decreased expression of the anti-inflammatory cytokines IL-10 and TNF-α. Finally, B cells from urinary bladder cancer patients, treated with a neoadjuvant regiment containing doxorubicin, displayed increased CD86-expression. We conclude that doxorubicin induces CD86 expression on B cells and hence enhances their antigen-presenting ability in vitro, a finding verified in patients. Development of tailored time and dose schedules may increase the effectiveness of combining chemotherapy and immunotherapy.

  • 30.
    Zirakzadeh, A. Ali
    et al.
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Kinn, Johan
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Krantz, David
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Rosenblatt, Robert
    Umeå Univ Hosp, Dept Surg & Perioperat Sci Urol & Androl, Umeå, Sweden; Karolinska Inst, Stockholm South Gen Hosp, Dept Urol, Stockholm, Sweden.
    Winerdal, Malin E.
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Hu, Jin
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Hartana, Ciputra Adijaya
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Lundgren, Christian
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Bergman, Emma Ahlén
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Johansson, Markus
    Sundsvall Hosp, Dept Urol, Sundsvall, Sweden.
    Holmström, Benny
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Hansson, Johan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Centrum för klinisk forskning, Gävleborg.
    Sidikii, Alexander
    Länssjukhuset Ryhov, Dept Urol, Region Jonköping, Sweden.
    Vasko, Janos
    Umeå Univ, Dept Med Biosci, Pathol, Umeå, Sweden.
    Marits, Per
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Sherif, Amir
    Umeå Univ Hosp, Dept Surg & Perioperat Sci Urol & Androl, Umeå, Sweden.
    Winqvist, Ola
    Karolinska Inst, Unit Immunol & Allergy, Dept Med, Stockholm, Sweden.
    Doxorubicin enhances the capacity of B cells to activate T cells in urothelial urinary bladder cancer2017Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 176, s. 63-70Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cancer is currently treated by a combination of therapies, including chemotherapy which is believed to suppress the immune system. Combination of immunotherapy and chemotherapy correlates with improved survival but needs careful planning in order to achieve a synergistic effect. In this study, we have demonstrated that doxorubicin treatment of B cells resulted in increased expression of CD86 and concordantly increased CD4(+) T cell activation in the presence of superantigen, an effect that was inhibited by the addition of a CD86 blocking antibody. Furthermore, doxorubicin resulted in decreased expression of the anti-inflammatory cytokines IL-10 and TNF-alpha. Finally, B cells from urinary bladder cancer patients, treated with a neoadjuvant regiment containing doxorubicin, displayed increased CD86-expression. We conclude that doxorubicin induces CD86 expression on B cells and hence enhances their antigen-presenting ability in vitro, a finding verified in patients. Development of tailored time and dose schedules may increase the effectiveness of combining chemotherapy and immunotherapy.

  • 31.
    Åkerman, Linda
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Ludvigsson, Johnny
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Barn- och kvinnocentrum, Barn- och ungdomskliniken i Linköping.
    Casas, Rosaura
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för kliniska vetenskaper. Linköpings universitet, Hälsouniversitetet.
    Low C-peptide levels and decreased expression of TNF and CD45 in children with high risk of type 1 diabetes2013Ingår i: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 148, nr 1Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Type 1 diabetes (T1D) patients have numeral and functional defects in peripheral immune cells, but the pre-diabetic period is fairly uncharacterized. Our aim was to analyze expression of immunological markers in T1D high risk children and relate it to clinical/immunological parameters. Children from ABIS (All Babies in Southeast Sweden) with greater than= 2 diabetes related autoantibodies were considered at high risk. Age-matched controls and new-onset T1D patients were included. Expression of genes related to immune cell function and different arms of the immune system was assessed in peripheral blood mononuclear cells using PCR array. Risk children had lower TNF and CD45, and although there were few differences between the groups, expression of many genes differed when comparing children with regard to residual insulin secretion. Hence, expression of immune related genes seemed related not only to the autoimmune process but rather to residual beta-cell function, which was decreased already during the pre-diabetic phase.

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