Ändra sökning
Avgränsa sökresultatet
1 - 37 av 37
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Träffar per sida
  • 5
  • 10
  • 20
  • 50
  • 100
  • 250
Sortering
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
  • Standard (Relevans)
  • Författare A-Ö
  • Författare Ö-A
  • Titel A-Ö
  • Titel Ö-A
  • Publikationstyp A-Ö
  • Publikationstyp Ö-A
  • Äldst först
  • Nyast först
  • Skapad (Äldst först)
  • Skapad (Nyast först)
  • Senast uppdaterad (Äldst först)
  • Senast uppdaterad (Nyast först)
  • Disputationsdatum (tidigaste först)
  • Disputationsdatum (senaste först)
Markera
Maxantalet träffar du kan exportera från sökgränssnittet är 250. Vid större uttag använd dig av utsökningar.
  • 1.
    Abdalla, Hana
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Forslund, Tony
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Schön, Thomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Stendahl, Olle
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Sundqvist, Tommy
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Medicinsk mikrobiologi. Linköpings universitet, Hälsouniversitetet.
    Effects of CNI-1493 on human granulocyte functions2006Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 211, nr 3, s. 191-197Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    During acute bacterial infections such as sepsis and meningitis, activation of inflammatory mediators such as nitric oxide (NO) plays a crucial role in both pathogenesis and host defense. We have previously reported that CNI-1493, a macrophage deactivator, reduced mortality in infant rats infected with Haemophilus influenzae type b (Hib) with associated decrease in the number of granulocytes in the infected tissue. The aim of the present study was to investigate how CNI-1493 affects granulocytes and macrophages in vitro. Murine macrophages (RAW 264.7) pre-incubated with CNI-1493 prior to activation with lipopolysaccharide (LPS)/interferon gamma (IFNγ) had decreased NO production measured as NO2/NO3 levels and reduction in inducible NO-synthase (iNOS) expression. Reactive oxygen species (ROS) production was increased in formylmethionyl-leucyl-phenylalanine (FMLP)-stimulated granulocytes following CNI-1493 treatment, whereas F-actin content, motility and chemotaxis were decreased under the same conditions. The effects of CNI-1493 on both NO production in LPS/IFNγ-activated macrophages and ROS production, F-actin content, motility and chemotaxis in granulocytes, may contribute to the reduced inflammatory response and increased survival in Hib-infected animals treated with CNI-1493.

  • 2. Barbosa-Lorenzi, Valéria C
    et al.
    Peyda, Simon
    Scheynius, Annika
    Nilsson, Gunnar
    Clincial Immunology and Allergy Unit, Department of Medicine Solna, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
    Lunderius-Andersson, Carolina
    Curdlan induces selective mast cell degranulation without concomitant release of LTC4, IL-6 or CCL22017Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 222, nr 4, s. 647-650, artikel-id S0171-2985(16)30455-7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Mast cells are sentinel cells with a tissue-specific localization in the interface between the host and the external environment. Their quick and selective response upon encountering pathogens is part of the innate host response and typically initiates the following adaptive immune response. Among several pattern recognition receptors (PRRs) involved in the recognition of pathogens by mast cells, the C-type lectin receptor Dectin-1 has been associated with the recognition of fungi. Our previous studies have shown that mast cells are the predominant cell type expressing Dectin-1 in human skin, and they also recognize and respond to Malassezia sympodialis by producing cytokines connected to the innate host response and upregulating the expression of Dectin-1. In the present study, we investigated mast cell responses to Curdlan, a β-glucan that acts as an agonist for the fungi receptor Dectin-1, and found a unique response pattern with induced degranulation, but surprisingly without synthesis of Leukotriene C4, IL-6 or CCL2. Since mast cells are the predominant Dectin-1 expressing cell in the human skin, this study suggests that mast cell degranulation in response to fungi is an important part of the first line of defense against these pathogens.

  • 3. Bratland, Eirik
    et al.
    Magitta, Ng'weina Francis
    Wolff, Anette Susanne Boe
    Ekern, Trude
    Knappskog, Per Morten
    Kämpe, Olle
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinska vetenskaper, Autoimmunitet.
    Haavik, Jan
    Husebye, Eystein Sverre
    Autoantibodies against aromatic amino acid hydroxylases in patients with autoimmune polyendocrine syndrome type 1 target multiple antigenic determinants and reveal regulatory regions crucial for enzymatic activity2013Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 218, nr 6, s. 899-909Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Patients with autoimmune polyendocrine syndrome type 1 (APS-1) frequently have autoantibodies directed against the aromatic amino acid hydroxylases tryptophan hydroxylase (TPH) and tyrosine hydroxylase (TH). We aimed to characterize these autoantibodies with regard to their antigenic determinants, their influence on enzymatic activity and their clinical associations. In particular, we wanted to compare autoantibodies against the two different isoforms of TPH, which display different tissue distribution. Using sera from 48 Scandinavian APS-1 patients we identified 36 patients (75%) with antibodies against one or more of these three enzymes. Antibodies against TPH1, but not TPH2, were associated with malabsorption in the whole Scandinavian cohort, while TH antibodies were associated with dental enamel hypoplasia in Norwegian patients. Subsequent experiments with selected patient sera indicated that while the C-terminal domain was the immunodominant part of TPH1, the epitopes of TPH2 and TH were mainly located in the N-terminal regulatory domains. We also identified a TPH1 specific epitope involved in antibody mediated inhibition of enzyme activity, a finding that provides new insight into the enzymatic mechanisms of the aromatic amino acid hydroxylases and knowledge about structural determinants of enzyme autoantigens. In conclusion, TPH1,TPH2 and TH all have unique antigenic properties in spite of their structural similarity. 

  • 4.
    Cholujová, Dana
    et al.
    Laboratory of Molecular Oncology, Cancer Research Institute, Slovak Academy of Sciences, Vlárska 7, Bratislava, Slovakia.
    Jakubíková, Jana
    Laboratory of Tumor Immunology, Cancer Research Institute, Slovak Academy of Sciences, Vlárska 7, Bratislava, Slovakia.
    Kubeš, Miroslav
    Institute of Virology, Slovak Academy of Sciences, Dubravska cesta 9, Bratislava, Slovakia.
    Arendacká, Barbora
    Institute of Measurement Science, Slovak Academy of Sciences, Dubravska cesta 9, Bratislava, Slovakia.
    Sapák, Michal
    Institute of Immunology, Medical Faculty of Comenius University, Sasinkova 4, Bratislava, Slovakia.
    Ihnatko, Robert
    Institute of Virology, Slovak Academy of Sciences, Dubravska cesta 9, Bratislava, Slovakia.
    Sedlák, Ján
    Laboratory of Tumor Immunology, Cancer Research Institute, Slovak Academy of Sciences, Vlárska 7, Bratislava, Slovakia.
    Comparative study of four fluorescent probes for evaluation of natural killer cell cytotoxicity assays2008Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 213, nr 8, s. 629-640Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Cytotoxicity is one of the major defence mechanisms against both virus-infected and tumor cells. Radioactive 51chromium (51Cr) release assay is a “gold standard” for assessment of natural killer (NK) cytolytic activity in vitro. Several disadvantages of this assay led us to design alternative tools based on flow cytometry analysis. Four different fluorescent dyes, calcein acetoxymethyl ester (CAM), carboxyfluorescein succinimidyl ester (CFSE), Vybrant DiO (DiO) and MitoTracker Green (MTG) were tested for labeling of NK target K-562 cells. Target staining stability, spontaneous release of fluorochromes and subsequent accumulation in bystander unstained cells were measured using fluorimetry and flow cytometry. Healthy donor peripheral blood mononuclear cells and affinity column purified NK cells were used as effectors coincubated with target K-562 cells at different E:T ratios for 3h and 90min, respectively. Fluorescent probe 7-amino-actinomycin D was used for live and dead cell discrimination. Bland–Altman statistical method was applied to measure true agreement for all CAM–51Cr, CFSE–51Cr, DiO–51Cr and MTG–51Cr pairs analyzed. Based on the data, none of the four proposed methods can be stated equivalent to the standard 51Cr release assay. Considering linear relationships between data obtained with four fluorochromes and 51Cr release assay as well as linear regression analysis with R2=0.9393 value for CAM–51Cr pair, we found the CAM assay to be the most closely related to the 51Cr assay.

  • 5.
    Ding, Zhoujie
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Bergman, Anna
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Rutemark, Christian
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    Heyman, Birgitta
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk biokemi och mikrobiologi.
    IgM-mediated enhancement of immune responses2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1177-1178Artikel i tidskrift (Övrigt vetenskapligt)
  • 6.
    Djedovic, Neda
    et al.
    Univ Belgrade, Serbia.
    Jevtic, Bojan
    Univ Belgrade, Serbia.
    Jose Mansilla, M.
    Germans Trias and Pujol Univ Hosp and Res Inst, Spain; Univ Autonoma Barcelona, Spain.
    Petkovic, Filip
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelning för neurobiologi. Linköpings universitet, Medicinska fakulteten. Univ Belgrade, Serbia.
    Blazevski, Jana
    Univ Belgrade, Serbia; Univ Oslo, Norway.
    Timotijevic, Gordana
    Univ Belgrade, Serbia.
    Navarro-Barriuso, Juan
    Germans Trias and Pujol Univ Hosp and Res Inst, Spain; Univ Autonoma Barcelona, Spain.
    Martinez-Caceres, Eva
    Germans Trias and Pujol Univ Hosp and Res Inst, Spain.
    Mostarica Stojkovide, Marija
    Univ Belgrade, Serbia.
    Miljkovic, Dorde
    Univ Belgrade, Serbia.
    Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats2019Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 224, nr 3, s. 470-476Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Dendritic cells (DC) are responsible for the initiation and shaping of the adaptive immune response and are in the focus of autoimmunity research. We were interested in comparison of DC obtained from autoimmunity-prone Dark Agouti (DA) rats and autoimmunity-resistant Albino Oxford (AO) rats. DC were generated from bone marrow precursors and matured (mDC) by lipopolysaccharide. Tolerogenic DC (tolDC) obtained by vitamin D3 treatment were studied in parallel. Profile of cytokine production was different in AO and DA mDC and tolDC. Expression of MHC class II molecules and CD86 were higher in DA DC, while vitamin D3 reduced their expression in dendritic cells of both strains. Allogeneic proliferation of CD4(+) T cells was reduced by AO tolDC, but not with DA tolDC in comparison to respective mDC. Finally, expression of various genes identified as differentially expressed in human mDC and tolDC was also analyzed in AO and DA DC. Again, AO and DA DC differed in the expression of the analyzed genes. To conclude, AO and DA DC differ in production of cytokines, expression of antigen presentation-related molecules and in regulation of CD4(+) T proliferation. The difference is valuable for understanding the divergence of the strains in their susceptibility to autoimmunity.

  • 7. Engberg, Anna E.
    et al.
    Nilsson, Per H.
    Mollnes, Tom Eirik
    Rosengren-Holmberg, Jenny P.
    Nicholls, Ian A.
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Ekdahl, Kristina Nilsson
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    The ratio between C4 and C4BP adsorbed from plasma predicts cytokine generation induced by artificial polymers in contact with whole blood2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1211-1211Artikel i tidskrift (Övrigt vetenskapligt)
  • 8.
    Engberg, Anna E.
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nilsson, Per H.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Mollnes, Tom Eirik
    Rosengren-Holmberg, Jenny P.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nicholls, Ian A.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nilsson, Bo
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    The ratio between C4 and C4BP adsorbed from plasma predicts cytokine generation induced by artificial polymers in contact with whole blood2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1211-1211Artikel i tidskrift (Övrigt vetenskapligt)
  • 9.
    Giusti, Pablo
    Stockholms universitet, Naturvetenskapliga fakulteten, Wenner-Grens institut, Avdelningen för immunologi.
    The novel anti-rheumatic compound Rabeximod impairs differentiation and function of human pro-inflammatory dendritic cells and macrophages2011Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 216, nr 1-2, s. 243-250Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Rabeximod (9-chloro-2,3-dimethyl-6-(N,N-dimethylaminoethylamino-2-oxoethyl)-6H-indolo[2,3-b]quinoxaline) is a synthetic compound that is currently being developed for the treatment of rheumatoid arthritis (RA). Here, we investigated the effects of Rabeximod on the functionality of human antigen-presenting cells (APCs) of myeloid origin. Different subsets of professional APCs were generated from human monocytes in vitro and simultaneously treated with different doses of Rabeximod. Although Rabeximod had no effect on the differentiation of monocytes into anti-inflammatory macrophages (AI-Ms), this compound impaired monocyte differentiation into monocyte-derived dendritic cells (MDCs) and pro-inflammatory allostimulated macrophages (Allo-Ms). MDCs that were treated with Rabeximod resulted in a significant decrease in their ability to pinocytose antigens, while no effect was exerted by the drug on the ability of Allo-Ms and AI-Ms to phagocytose. Furthermore, we observed a significant reduction in the allostimulatory ability of MDCs and Allo-Ms after treatment with Rabeximod, although this compound did not affect the low immunostimulatory capacity of AI-Ms. Conversely, the effect of Rabeximod in influencing cytokine secretion by APCs appeared to be limited. In conclusion, Rabeximod impairs differentiation of monocytes into different pro-inflammatory APCs, leading to impaired immunostimulatory abilities of these cells. Our observations shed light on the cellular mode of action and the immunomodulatory effect of Rabeximod.

  • 10.
    Hamad, Osama A.
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för onkologi, radiologi och klinisk immunologi, Enheten för klinisk immunologi.
    Ekdahl, Kristina N
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Non-proteolytically activated C3 promotes binding of activated platelets and platelet-derived microparticles to leukocytes via CD11b/CD182012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1191-1191Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background:

    We have previously demonstrated that complement component C3 binds to the surface of activated platelets, independent of proteolytic activation. The resulting form of C3, termed C3(H2O), was shown to be a ligand for recombinant CD35 (complement receptor 1, CR1). Previous studies by others have indicated that platelet-leukocyte complex (PLC) formation is dependent on the interaction between platelet exposed P-selectin (CD62P) and its ligand, PSGL-1, on leukocytes. In addition, CD11b/CD18 (Mac-1 or CR3) has been shown to participate in this reaction, but its ligand has not yet been identified.

    Objective:

    To test the hypothesis that C3 bound to activated platelets and platelet-derived microparticles (PMPs) can act as a ligand for CD11b/CD18 (CR3) and contribute to PLC formation.

    Methods and results:

    Blood cells were depleted of plasma proteins. After extensive washing, C3 was added, and the leukocytes were activated with C5a and the platelets with thrombin receptor-activating peptide (TRAP). PLC formation was detected by flow cytometry (monocytes: CD14+/CD42a+, granulocytes: CD16+/CD42a+). For both granulocytes and monocytes, the addition of C3 significantly enhanced PLC formation. Formation of PLC was inhibited by both anti-P-selectin and anti-CD11b monoclonal antibodies. In addition, PMPs isolated from serum, were found to expose C3(H2O) and bind to leukocytes in a fashion similar to activated platelets.

    Conclusion:

    We have identified proteolytically non-activated C3 as a ligand for CD11b in the formation of PLC and possibly the binding of PMPs to leukocytes. This observation most likely has pathophysiological implications for the recently reported links between thrombotic disease and the complement system.

  • 11. Hamad, Osama A.
    et al.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nilsson, Bo
    Non-proteolytically activated C3 promotes binding of activated platelets and platelet-derived microparticles to leukocytes via CD11b/CD182012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1191-1191Artikel i tidskrift (Övrigt vetenskapligt)
  • 12.
    Harboe, M.
    et al.
    Oslo University Hospital Rikshospitalet, Norway.
    Johnson, C.
    Oslo University Hospital Rikshospitalet, Norway.
    Nymo, S.
    Nordland Hospital, Norway.
    Ekholt, K.
    Oslo University Hospital Rikshospitalet, Norway.
    Schjalm, C.
    Oslo University Hospital Rikshospitalet, Norway.
    Lindstad, J. K.
    Oslo University Hospital Rikshospitalet, Norway.
    Pharo, A.
    Oslo University Hospital Rikshospitalet, Norway.
    Hellerud, B. C.
    Oslo University Hospital Rikshospitalet, Norway.
    Nilsson Ekdahl, Kristina
    Uppsala University.
    Mollnes, T. E.
    Oslo University Hospital Rikshospitalet, Norway ; Nordland Hospital, Norway.
    Nilsson, Per H.
    Oslo University Hospital Rikshospitalet, Norway.
    Molecular modelling showed optimal fit between TSR5 in trimeric properdin and C345C in the C3b moiety for stabilization of the alternative convertase, whereas binding to molecular patterns in myeloperoxidase, endothelial cells and Neisseria meningitides was indirectly mediated by initial C3 activation2016Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 221, nr 10, s. 1205-1205Artikel i tidskrift (Refereegranskat)
  • 13.
    Harboe, Morten
    et al.
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway..
    Johnson, Christina
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway..
    Nymo, Stig
    Nordland Hosp, Res Lab, Bodo, Norway..
    Ekholt, Karin
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway..
    Schjalm, Camilla
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway..
    Lindstad, Julie K.
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway..
    Pharo, Anne
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway..
    Hellerud, Bernt C.
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway..
    Ekdahl, Kristina N.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Mollnes, Tom E.
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway.;Nordland Hosp, Res Lab, Bodo, Norway..
    Nilsson, Per H.
    Natl Hosp Norway, Oslo Univ Hosp, Dept Immunol, Oslo, Norway..
    Molecular modelling showed optimal fit between TSR5 in trimeric properdin and C345C in the C3b moiety for stabilization of the alternative convertase, whereas binding to molecular patterns in myeloperoxidase, endothelial cells and Neisseria meningitides was indirectly mediated by initial C3 activation2016Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 221, nr 10, s. 1205-1205Artikel i tidskrift (Övrigt vetenskapligt)
  • 14. Huang, Shan
    et al.
    Nilsson, Per H.
    Sandholm, Kerstin
    Elmlund, Louise
    Nicholls, Ian A.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Kemiska sektionen, Institutionen för kemi - BMC, Fysikalisk-organisk kemi.
    Ekdahl, Kristina Nilsson
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Regulation of complement in whole blood by heparin molecularly imprinted polymer particles2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1199-1199Artikel i tidskrift (Övrigt vetenskapligt)
  • 15.
    Huang, Shan
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nilsson, Per H.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Sandholm, Kerstin
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Elmlund, Louise
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nicholls, Ian A.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Regulation of complement in whole blood by heparin molecularly imprinted polymer particles2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1199-1199Artikel i tidskrift (Övrigt vetenskapligt)
  • 16. Klapper, Yvonne
    et al.
    Hamad, Osama
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi.
    Teramura, Yuji
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Leneweit, Gero
    Nienhaus, Gerd Ulrich
    Ekdahl, Kristina Nilsson
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Investigation of complement activation by neutral liposomes2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1179-1180Artikel i tidskrift (Övrigt vetenskapligt)
  • 17. Klapper, Yvonne
    et al.
    Hamad, Osama
    Teramura, Yuji
    Leneweit, Gero
    Nienhaus, Gerd Ulrich
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nilsson, Bo
    Investigation of complement activation by neutral liposomes2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1179-1180Artikel i tidskrift (Övrigt vetenskapligt)
  • 18.
    Kozarcanin, Huda
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Ekdahl, Kristina Nilsson
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    The lectin pathway triggered by activated platelets2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1130-1130Artikel i tidskrift (Övrigt vetenskapligt)
  • 19.
    Kulak, Klaudia
    et al.
    Lund Univ, Dept Translat Med, Sect Med Prot Chem, S-20502 Malmo, Sweden..
    Westermark, Gunilla
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Papac-Milicevic, Nikolina
    Med Univ Vienna, Dept Lab Med, Vienna, Austria..
    Renström, Erik
    Lund Univ, Ctr Diabet, Dept Clin Sci Malmo, S-20502 Malmo, Sweden..
    Blom, Anna M.
    Lund Univ, Dept Translat Med, Sect Med Prot Chem, S-20502 Malmo, Sweden..
    King, Ben C.
    Lund Univ, Dept Translat Med, Sect Med Prot Chem, S-20502 Malmo, Sweden..
    The complement regulator C4b-binding protein inhibits islet amyloid polypeptide-induced inflammasome activation2016Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 221, nr 10, s. 1162-1162Artikel i tidskrift (Övrigt vetenskapligt)
  • 20.
    López-González, Moisés
    et al.
    Stockholms universitet, Naturvetenskapliga fakulteten, Institutionen för molekylär biovetenskap, Wenner-Grens institut. Av. IPN, México.
    Meza-Sanchez, David
    Garcia-Cordero, Julio
    Bustos-Arriaga, Jose
    Velez-Del Valle, Cristina
    Marsch-Moreno, Meytha
    Castro-Jimenez, Tannya
    Flores-Romo, Leopoldo
    Santos-Argumedo, Leopoldo
    Gutierrez-Castaneda, Benito
    Cedillo-Barróna, Leticia
    Human keratinocyte cultures (HaCaT) can be infected by DENV, triggering innate immune responses that include IFN lambda and LL372018Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 223, nr 11, s. 608-617Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The skin is the first anatomical region that dengue virus (DENV) encounters during the natural infection. Although the role of some skin resident cells like dendritic cells and fibroblasts has been demonstrated to be crucial to elucidate the role of resident cells and molecules participating during the early events of the innate immune response, the participation of keratinocytes during DENV infection has not been fully elucidated. In this paper we aimed to evaluate the use of the HaCaT cell line as a model to study the immune responses of skin keratinocytes to DENV infection. We demonstrated productive DENV-2 infection of HaCaT cells and their capability to establish an antiviral response through production of type I and type III interferons (IFN-beta and IFN-lambda). The production of these cytokines by HaCaT cells correlated with upregulation of IFN-inducible transmembrane protein-3 (IFITM3) and viperin in bystander, uninfected cells. We also observed an increase in secretion of IL-6 and IL-8. Skin keratinocytes are known to secrete antimicrobial peptides (AMPs) during viral infections. In our model, DENV-2 infected HaCaT cells upregulate the production of cytoplasmic LL-37. We evaluated the dual role of LL-37, HBD2, and HBD3 antiviral activity and immunoregulation during DENV-2 infection of HaCaT cells and found that LL-37 significantly reduced DENV-2 replication. This indicates that the HaCaT cell line can be used as a model for studying the innate response of keratinocytes to DENV infection. Our results also suggest that skin keratinocytes play an important role in the skin microenvironment after DENV infection by secreting molecules like type I and type III IFNs, pro-inflammatory molecules, and LL-37, which may contribute to the protection against arboviral infections.

  • 21.
    Nilsson, Bo
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Ekdahl, Kristina Nilsson
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    The tick-over theory revisited: Is C3 a contact-activated protein?2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1106-1110Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The tick-over theory was first introduced in the 1970s to explain the presence of the initial C3b molecules, which are able to trigger complement activation by the alternative pathway in human plasma under physiological conditions. After the identification of the thioester, the predominant hypothesis has been that this bond is hydrolyzed at a slow but constant rate by nucleophilic attack by H2O, leading to the generation of C3(H2O). Here we put forward the hypothesis that the rate of hydrolysis of C3 to C3(H2O) may be greatly accelerated by the interaction between C3 and a number of biological and artificial interfaces, including gas bubbles, biomaterial surfaces and different lipid surfaces and complexes. We therefore propose that C3 should preferentially be regarded as a contact activated protein rather than a target for passive, random hydrolysis in the fluid phase.

  • 22. Nilsson, Bo
    et al.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    The tick-over theory revisited: Is C3 a contact-activated protein?2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1106-1110Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The tick-over theory was first introduced in the 1970s to explain the presence of the initial C3b molecules, which are able to trigger complement activation by the alternative pathway in human plasma under physiological conditions. After the identification of the thioester, the predominant hypothesis has been that this bond is hydrolyzed at a slow but constant rate by nucleophilic attack by H2O, leading to the generation of C3(H2O). Here we put forward the hypothesis that the rate of hydrolysis of C3 to C3(H2O) may be greatly accelerated by the interaction between C3 and a number of biological and artificial interfaces, including gas bubbles, biomaterial surfaces and different lipid surfaces and complexes. We therefore propose that C3 should preferentially be regarded as a contact activated protein rather than a target for passive, random hydrolysis in the fluid phase. (C) 2012 Elsevier GmbH. All rights reserved.

  • 23.
    Nilsson Ekdahl, Kristina
    et al.
    Linnéuniversitetet, Fakulteten för Hälso- och livsvetenskap (FHL), Institutionen för kemi och biomedicin (KOB). Uppsala University.
    Teramura, Yuji
    Uppsala University;Univ Tokyo, Japan.
    Asir, Sana
    Uppsala University.
    Manell, Elin
    Swedish University of Agricultural Sciences.
    Biglarnia, Alireza
    Skåne Univ Hosp.
    Jensen-Waern, Marianne
    Swedish University of Agricultural Sciences.
    Nilsson, Bo
    Uppsala University.
    Protective role of PEG conjugated phospholipid in reducing ischemic reperfusion injury in two allogeneic pig kidney transplant models2016Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 221, nr 10, s. 1184-1184Artikel i tidskrift (Övrigt vetenskapligt)
  • 24.
    Orrem, H. L.
    et al.
    Oslo University Hospital, Norway ; University of Oslo, Norway.
    Nilsson, Per H.
    Oslo University Hospital, Norway ; University of Oslo, Norway.
    Barratt-Due, A.
    Oslo University Hospital, Norway.
    Pische, S. E.
    Oslo University Hospital, Norway.
    Grindheim, G.
    Rikshospitalet, Oslo University Hospital, Norway.
    Garred, P.
    University of Copenhagen, Denmark.
    Husebye, T.
    Oslo University Hospital Ullevål, Norway ; University of Oslo, Norway.
    Andersen, G. O.
    Oslo University Hospital Ullevål, Norway ; University of Oslo, Norway.
    Mollnes, T. E.
    Oslo University Hospital, Norway ; University of Oslo, Norway ; Research Laboratory Nordland Hospital, Norway ; University of Tromsø, Norway ; Norwegian University of Science and Technology, Norway.
    Complement activation in acute heart failure following myocardial infarction2016Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 221, nr 10, s. 1203-1204Artikel i tidskrift (Refereegranskat)
  • 25.
    Otterdal, K.
    et al.
    Oslo University Hospital Rikshospitalet, Norway.
    Portillo, A.
    Hospital San Pedro-Center of Biomedical Research from La Rioja (CIBIR), Spain.
    Astrup, E.
    Oslo University Hospital Rikshospitalet, Norway.
    Ludviksen, J. K.
    Nordland Hospital, Norway.
    Schjalm, C.
    Oslo University Hospital Rikshospitalet, Norway.
    Raoult, D.
    Université de la Mediterranée, France.
    Olano, J. P.
    University of Texas Medical Branch, USA.
    Halvorsen, B.
    Oslo University Hospital Rikshospitalet, Norway.
    Oteo, J. A.
    Hospital San Pedro-Center of Biomedical Research from La Rioja (CIBIR), Spain.
    Aukrust, P.
    Oslo University Hospital Rikshospitalet, Norway.
    Mollnes, T. E.
    Nordland Hospital, Norway ; Oslo University Hospital Rikshospitalet, Norway.
    Nilsson, Per H.
    Oslo University Hospital Rikshospitalet, Norway.
    Rickettsia conorii is a potent complement activator in vivo and combined inhibition of complement and CD14 is required for attenuation of the cytokine response ex vivo2016Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 221, nr 10, s. 1204-1205, artikel-id 161Artikel i tidskrift (Refereegranskat)
  • 26.
    Prohaszka, Zoltan
    et al.
    Semmelweis Univ, Dept Internal Med 3, Res Lab, Budapest, Hungary.;Semmelweis Univ, Fust Gyorgy Complement Diagnost Lab, Budapest, Hungary..
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Frazer-Abel, Ashley
    Natl Jewish Hlth, Complement Lab, Denver, CO USA..
    Kirschfink, Michael
    Heidelberg Univ, Inst Immunol, Neuenheimer Feld 305, D-69120 Heidelberg, Germany..
    Complement analysis 2016: Clinical indications, laboratory diagnostics and quality control2016Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 211, nr 11, s. 1247-1258Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In recent years, complement analysis of body fluids and biopsies, going far beyond C3 and C4, has significantly enhanced our understanding of the disease process. Such expanded complement analysis allows for a more precise differential diagnosis and for critical monitoring of complement-targeted therapy. These changes are a result of the growing understanding of the involvement of complement in a diverse set of disorders. To appreciate the importance of proper complement analysis, it is important to understand the role it plays in disease. Historically, it was the absence of complement as manifested in severe infection that was noted. Since then complement has been connected to a variety of inflammatory disorders, such as autoimmune diseases and hereditary angioedema. While the role of complement in the rejection of renal grafts has been known longer, the significant impact of complement. In certain nephropathies has now led to the reclassification of some rare kidney diseases and an increased role for complement analysis in diagnosis. Even more unexpected is that complement has also been implicated in neural, ophtalmological and dermatological disorders. With this level of involvement in some varied and impactful health issues proper complement testing is clearly important; however, analysis of the complement system varies widely among laboratories. Except for a few proteins, such as C3 and C4, there are neither well-characterized standard preparations nor calibrated assays available. This is especially true for the inter-laboratory variation of tests which assess classical, alternative, or lectin pathway function. In addition, there is a need for the standardization of the measurement of complement activation products that are so critical in determining whether clinically relevant complement activation has occurred in vivo. Finally, autoantibodies to complement proteins (e.g. anti-C1q), C3 and C4 convertases (C3 and C4 nephritic factor) or to regulatory proteins (e.g. anti-Clinhibitor, anti-factor H) are important in defining autoimmune processes and diseases based on complement dysregulation. To improve the quality of complement laboratory analysis a standardization commmittee of the International Complement Society (ICS) and the International Union of Immunological Societies (IUIS) was formed to provide guidelines for modern complement analysis and standards for the development of international testing programs.

  • 27. Sandholm, Kerstin
    et al.
    Henningsson, Anna J.
    Bergstrom, Sven
    Ernerudh, Jan
    Ekdahl, Kristina Nilsson
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Complement activation and phagocytosis in vitro of two strains of Borrelia burgdorferi S.L2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1153-1153Artikel i tidskrift (Övrigt vetenskapligt)
  • 28.
    Sandholm, Kerstin
    et al.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Henningsson, Anna J.
    Bergstrom, Sven
    Ernerudh, Jan
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Complement activation and phagocytosis in vitro of two strains of Borrelia burgdorferi S.L2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1153-1153Artikel i tidskrift (Övrigt vetenskapligt)
  • 29. Sandholm, Kerstin
    et al.
    Henningsson, Anna J.
    Bergström, Sven
    Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten).
    Ernerudh, Jan
    Ekdahl, Kristina Nilsson
    Complement activation and phagocytosis in vitro of two strains of Borrelia burgdorferi S.L2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1153-1153Artikel i tidskrift (Övrigt vetenskapligt)
  • 30. Sjölander, Jonatan
    et al.
    Lundmark, Katarzyna
    Wetsel, Rick
    Blom, Anna M.
    Westermark, Gunilla T.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för medicinsk cellbiologi.
    Complement inhibitor C4b-binding protein is involved in protein AA amyloidosis2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1158-1158Artikel i tidskrift (Övrigt vetenskapligt)
  • 31.
    Skjoedt, Mikkel-Ole
    et al.
    Univ Copenhagen, Fac Hlth & Med Sci, Rigshosp, Lab Mol Med,Dept Clin Immunol,Sect 7631, DK-1168 Copenhagen, Denmark.;Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury, Boston, MA 02115 USA..
    Pavlov, Vasile
    Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury, Boston, MA 02115 USA..
    Kozarcanin, Huda
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Willer, Anton
    Univ Copenhagen, Fac Hlth & Med Sci, Rigshosp, Lab Mol Med,Dept Clin Immunol,Sect 7631, DK-1168 Copenhagen, Denmark..
    Munthe-Fog, Lea
    Univ Copenhagen, Fac Hlth & Med Sci, Rigshosp, Lab Mol Med,Dept Clin Immunol,Sect 7631, DK-1168 Copenhagen, Denmark..
    Hansen, Karin Moller
    Univ Copenhagen, Fac Hlth & Med Sci, Rigshosp, Lab Mol Med,Dept Clin Immunol,Sect 7631, DK-1168 Copenhagen, Denmark..
    Nilsson-Ekdahl, Kristina
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Stahl, Gregory L.
    Harvard Univ, Brigham & Womens Hosp, Ctr Expt Therapeut & Reperfus Injury, Boston, MA 02115 USA..
    Garred, Peter
    Univ Copenhagen, Fac Hlth & Med Sci, Rigshosp, Lab Mol Med,Dept Clin Immunol,Sect 7631, DK-1168 Copenhagen, Denmark..
    The lectin complement pathway inhibitor MAP-1 is an upstream regulator of the coagulation cascade2016Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 221, nr 10, s. 1209-1209Artikel i tidskrift (Övrigt vetenskapligt)
  • 32.
    Skoglund, Caroline
    et al.
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    Wetterö, Jonas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Reumatologi. Linköpings universitet, Hälsouniversitetet.
    Tengvall, Pentti
    Linköpings universitet, Institutionen för fysik, kemi och biologi, Tillämpad Fysik. Linköpings universitet, Tekniska högskolan.
    Bengtsson, Torbjörn
    Linköpings universitet, Institutionen för medicin och hälsa, Farmakologi. Linköpings universitet, Hälsouniversitetet.
    C1q induces a rapid up-regulation of P-selectin and modulates collagen- and collagen-related peptide-triggered activation in human platelets2010Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 215, nr 12, s. 987-995Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Blood platelets are emerging as important immunomodulatory cells, but complement interaction with platelets is not well understood. Several platelet structures have been described as complement protein 1q (C1q) binding receptors, such as C1qRp/CD93 and gC1qR. However, there are conflicting results whether these receptors are C1q binding structures, or even at all expressed on the cell surface. Recently, the collagen-binding integrin alphaIIbetaI was reported to bind C1q on mast cells, and this receptor is also present on platelets. The aim of this study was to further characterize the effects of C1q on platelets, by quantifying the platelet surface expression of P-selectin (CD62P) and monitoring the formation of platelet-neutrophil aggregates. Using flow cytometry, we found that C1q dose-dependently triggered a rapid but moderate and transient up-regulation of P-selectin already within 5s of C1q exposure. Pre-incubation with an antibody directed against gC1qR significantly inhibited (with 57% compared to control) the up-regulation, whereas an antibody towards the alphaIIbetaI-integrin showed no effect. Stimulation with C1q did not change the cytosolic calcium-levels, as measured with the fluorescent ratiometric probe Fura-2, however, a protein kinase C inhibitor (GF109203x) blocked the C1q-induced P-selectin expression. Furthermore, pre-incubation of platelets with C1q diminished both the collagen as well as the collagen-related peptide-induced up-regulation of P-selectin, most evident after 90s of stimulation. This indicates that C1q may regulate platelet activation via the GPVI receptor, which is a novel finding. Moreover, C1q antagonized the collagen-induced formation of platelet-neutrophil aggregates, indicating a reduced interaction between platelet P-selectin and neutrophil P-selectin glycoprotein ligand-1(PSGL-1/CD162). In summary, C1q induces a moderate rapid platelet P-selectin expression, modulates subsequent collagen and collagen-related peptide stimulation of platelets, and inhibits the formation of platelet-neutrophil aggregates. These immuno-regulatory effects of C1q may have a crucial role in innate immunity and inflammation.

  • 33.
    Skoglund, Caroline
    et al.
    Div Drug Res, Dept Med & Hlth Sci, Linkoping Univ, Linkoping, Sweden.
    Wetterö, Jonas
    Rheumatol Autoimmun & Immune Regulat Unit, Dept Clin & Expt Med, Linkoping Univ, Linkoping, Sweden.
    Tengvall, Pentti
    Inst Clin Sci, Dept Biomat, Sahlgrenska Acad, Univ Gothenburg, Gothenburg, Sweden.
    Bengtsson, Torbjörn
    Örebro universitet, Hälsoakademin. Div Drug Res, Dept Med & Hlth Sci, Linkoping Univ, Linkoping, Sweden.
    C1q induces a rapid up-regulation of P-selectin and modulates collagen- and collagen-related peptide-triggered activation in human platelets2010Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 215, nr 12, s. 987-995Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Blood platelets are emerging as important immunomodulatory cells, but complement interaction with platelets is not well understood. Several platelet structures have been described as complement protein 1q (C1q) binding receptors, such as C1qRp/CD93 and gC1qR. However, there are conflicting results whether these receptors are C1q binding structures, or even at all expressed on the cell surface. Recently, the collagen-binding integrin alpha II beta I was reported to bind C1q on mast cells, and this receptor is also present on platelets. The aim of this study was to further characterize the effects of C1q on platelets, by quantifying the platelet surface expression of P-selectin (CD62P) and monitoring the formation of platelet-neutrophil aggregates. Using flow cytometry, we found that C1q dose-dependently triggered a rapid but moderate and transient up-regulation of P-selectin already within 5s of C1q exposure. Pre-incubation with an antibody directed against gC1qR significantly inhibited (with 57% compared to control) the up-regulation, whereas an antibody towards the alpha II beta I-integrin showed no effect. Stimulation with C1q did not change the cytosolic calcium-levels, as measured with the fluorescent ratiometric probe Fura-2, however, a protein kinase C inhibitor (GF109203x) blocked the C1q-induced P-selectin expression. Furthermore, pre-incubation of platelets with C1q diminished both the collagen as well as the collagen-related peptide-induced up-regulation of P-selectin, most evident after 90 s of stimulation. This indicates that C1q may regulate platelet activation via the GPVI receptor, which is a novel finding. Moreover, C1q antagonized the collagen-induced formation of platelet-neutrophil aggregates, indicating a reduced interaction between platelet P-selectin and neutrophil P-selectin glycoprotein ligand-1(PSGL-1/CD162). In summary, C1q induces a moderate rapid platelet P-selectin expression, modulates subsequent collagen and collagen-related peptide stimulation of platelets, and inhibits the formation of platelet-neutrophil aggregates. These immuno-regulatory effects of C1q may have a crucial role in innate immunity and inflammation. (C) 2009 Elsevier GmbH. All rights reserved.

  • 34.
    Svärd, Anna
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Hälsouniversitetet.
    Kastbom, Alf
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Reumatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Sommarin, Yngve
    Euro-Diagnostica AB, Malmö, Sweden.
    Skogh, Thomas
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Reumatologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Hjärt- och Medicincentrum, Reumatologiska kliniken i Östergötland.
    Salivary IgA antibodies to cyclic citrullinated peptides (CCP) in rheumatoid arthritis2013Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 218, nr 2, s. 232-237Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Circulating IgG anti-cyclic citrullinated peptide antibodies (CCP) are highly specific for rheumatoid arthritis (RA) and prognostic of poor outcome. Serum IgA anti-CCP occurs in a subset of IgG-positive cases and relates to still more aggressive disease. Mucosal IgA-class antibodies, however, are generally associated with anti-inflammatory actions and systemic tolerance induction. In the present study, unstimulated salivary samples from 63 patients with established RA and 20 healthy persons were analysed by enzyme-linked immunoassay for the presence of IgA anti-CCP antibodies. To ensure antigen specificity, IgA-reactivity with the corresponding uncitrullinated antigen, cyclic arginine peptide (CAP), was analysed and anti-CCP/anti-CAP ratios calculated. Retrospective data regarding disease activity and radiological outcome were achieved via medical records. Salivary IgA anti-CCP was found in 14/63 (22%) patients and one (5%) control (positive test = anti-CCP/anti-CAP ratio andgt; 1.5). Salivary IgA reactivity was dose-dependently inhibited by pre-incubation with soluble CCP to a degree strongly correlating with anti-CCP/anti-CAP ratio. In salivary IgA anti-CCP positive patients, joint erosions within 6 years of diagnosis was significantly lower (p = 0.043), and at the time for diagnosis there was a trend towards lower erythrocyte sedimentation rate (p = 0.071) and C-reactive protein (p = 0.085). Contrasting to circulating IgG and IgA anti-CCP, our results imply that salivary IgA antibodies may be associated with a less severe outcome of RA. Hypothetically, this relates to an anti-inflammatory and protective immunomodulating role of secretory IgA-class autoantibodies against citrullinated antigens presented at mucosal surfaces.

  • 35.
    Teramura, Yuji
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Nilsson, Per H.
    Ekdahl, Kristina N.
    Magnusson, Peetra U.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Qu, Hongchang
    Ricklin, Daniel
    Hong, Jaan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Lambris, John D.
    Nilsson, Bo
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för immunologi, genetik och patologi, Klinisk immunologi.
    Autoregulation of thromboinflammation on biomaterials and cells by a novel therapeutic coating technique2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1140-1140Artikel i tidskrift (Övrigt vetenskapligt)
  • 36. Teramura, Yuji
    et al.
    Nilsson, Per H.
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Nilsson Ekdahl, Kristina
    Linnéuniversitetet, Fakultetsnämnden för naturvetenskap och teknik, Institutionen för naturvetenskap, NV.
    Magnusson, Peetra U.
    Qu, Hongchang
    Ricklin, Daniel
    Hong, Jaan
    Lambris, John D.
    Nilsson, Bo
    Autoregulation of thromboinflammation on biomaterials and cells by a novel therapeutic coating technique2012Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 217, nr 11, s. 1140-1140Artikel i tidskrift (Övrigt vetenskapligt)
  • 37.
    Wu, Chenglin
    et al.
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för organismbiologi, Jämförande fysiologi.
    Charoensapsri, Walaiporn
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för organismbiologi, Jämförande fysiologi.
    Nakamura, Seiko
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för organismbiologi, Jämförande fysiologi.
    Tassanakajon, Anchalee
    Center of Excellence for Molecular Biology and Genomics of Shrimp, Department of Biochemistry, Faculty of Science, Chulalongkorn University.
    Söderhäll, Irene
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för organismbiologi, Jämförande fysiologi.
    Söderhäll, Kenneth
    Uppsala universitet, Teknisk-naturvetenskapliga vetenskapsområdet, Biologiska sektionen, Institutionen för organismbiologi, Jämförande fysiologi.
    An MBL-like protein may interfere with the activation of the proPO-system, an important innate immune reaction in invertebrates2013Ingår i: Immunobiology, ISSN 0171-2985, E-ISSN 1878-3279, Vol. 218, nr 2, s. 159-168Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    An important characteristic of the innate immune systems of crayfish and other arthropods is the activation of a serine proteinase cascade in the hemolymph, which results in the activation of prophenoloxidase and subsequently leading to the formation of toxic quinones and melanin. Although no true complement homologues have been detected in crayfish or crustaceans, several proteins with similarities to vertebrate pattern recognition receptors (PRRs), which are involved in the lectin pathway of complement activation in vertebrates, are present. One is a C-type lectin, a mannose-binding lectin (Pl-MBL), which is secreted from granular hemocytes. Here we report that Pl-MBL has LPS-binding capacity and is dependent upon high Ca(2+) for its solubility and Pl-MBL interferes with proPO activation in vitro when HLS is prepared at high Ca(2+). The proPO-activating system is efficiently activated by microbial polysaccharides and it has to be neatly regulated to avoid activation in places where it is inappropriate and the active enzyme PO should be prevented from spreading throughout the body of the animal. This may be particularly important during molting when proPO is involved in hardening of a new cuticle and the animal is vulnerable to microbes. The presence of high amount of Pl-MBL in the granular hemocytes may play a role in this process. Since a hemocyte lysate supernatant (HLS) prepared at 100mM Ca(2+) could become activated when the concentration of LPS was increased up to 3mg/ml, this may indicate that Pl-MBL acts as a scavenger for LPS to prevent spreading of LPS in the hemolymph to avoid further activation of the proPO-system.

1 - 37 av 37
RefereraExporteraLänk till träfflistan
Permanent länk
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annat format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annat språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf