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  • 1.
    Hage, C. Camilla
    et al.
    Karolinska Inst, Dept Med, Stockholm, Sweden..
    Lofström, U.
    Corbiasco, M.
    Karolinska Univ Hosp, Stockholm, Sweden..
    Eriksson, M.
    Karolinska Univ Hosp, Stockholm, Sweden..
    Persson, Barbro
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology. Karolinska Inst, Sci Life Lab, Uppsala, Sweden..
    Wallen, H.
    Danderyd Hosp, Stockholm, Sweden..
    Persson, H.
    Danderyd Hosp, Stockholm, Sweden..
    Linde, C.
    Karolinska Inst, Dept Med, Stockholm, Sweden..
    Rationale: preserved and reduced ejection fraction epidemiological regional study in stockholm (PREFERS)2015In: European Journal of Heart Failure, ISSN 1388-9842, E-ISSN 1879-0844, Vol. 17, p. 302-302Article in journal (Other academic)
  • 2.
    Manivel, Vivek Anand
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Mullazehi, Mohammed
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Sohrabian, Azita
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Persson, Barbro
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Elshafie, Amir
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Kavvadas, Efstathios
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Rönnelid, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Neutrophil Granulocytes Respond to Surface-Bound Immune Complexes Containing Anti-Type II Collagen Antibodies from RA Patients2013In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 72, p. A39-A39Article in journal (Other academic)
  • 3.
    Mohebnasab, Maedeh
    et al.
    Univ Penn, Dept Surg, Div Transplantat, Philadelphia, PA 19104 USA.
    Eriksson, Oskar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Persson, Barbro
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Sandholm, Kerstin
    Linnaeus Univ, Ctr Biomat Chem, Kalmar, Sweden.
    Mohlin, Camilla
    Linnaeus Univ, Ctr Biomat Chem, Kalmar, Sweden.
    Huber-Lang, Markus
    Univ Hosp Ulm, Inst Clin & Expt Trauma Immunol, Ulm, Germany.
    Keating, Brendan J.
    Univ Penn, Dept Surg, Div Transplantat, Philadelphia, PA 19104 USA.
    Nilsson Ekdahl, Kristina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology. Linnaeus Univ, Ctr Biomat Chem, Kalmar, Sweden.
    Nilsson, Bo
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Current and Future Approaches for Monitoring Responses to Anti-complement Therapeutics2019In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, article id 2539Article, review/survey (Refereed)
    Abstract [en]

    Aberrations in complement system functions have been identified as either direct or indirect pathophysiological mechanisms in many diseases and pathological conditions, such as infections, autoimmune diseases, inflammation, malignancies, and allogeneic transplantation. Currently available techniques to study complement include quantification of (a) individual complement components, (b) complement activation products, and (c) molecular mechanisms/function. An emerging area of major interest in translational studies aims to study and monitor patients on complement regulatory drugs for efficacy as well as adverse events. This area is progressing rapidly with several anti-complement therapeutics under development, in clinical trials, or already in clinical use. In this review, we summarized the appropriate indications, techniques, and interpretations of basic complement analyses, exemplified by a number of clinical disorders.

  • 4.
    Nilsson Ekdahl, Kristina
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology. Linnaeus Univ, Ctr Biomat Chem, Kalmar, Sweden.
    Persson, Barbro
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Mohlin, Camilla
    Linnaeus Univ, Ctr Biomat Chem, Kalmar, Sweden.
    Sandholm, Kerstin
    Linnaeus Univ, Ctr Biomat Chem, Kalmar, Sweden.
    Skattum, Lillemor
    Lund Univ, Dept Lab Med Clin Immunol & Transfus Med, Sect Microbiol Immunol & Glycobiol, Lund, Sweden.
    Nilsson, Bo
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Interpretation of Serological Complement Biomarkers in Disease2018In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 9, article id 2237Article, review/survey (Refereed)
    Abstract [en]

    Complement systemaberrations have been identified as pathophysiological mechanisms in a number of diseases and pathological conditions either directly or indirectly. Examples of such conditions include infections, inflammation, autoimmune disease, as well as allogeneic and xenogenic transplantation. Both prospective and retrospective studies have demonstrated significant complement-related differences between patient groups and controls. However, due to the low degree of specificity and sensitivity of some of the assays used, it is not always possible to make predictions regarding the complement status of individual patients. Today, there are three main indications for determination of a patient's complement status: (1) complement deficiencies (acquired or inherited); (2) disorders with aberrant complement activation; and (3) C1 inhibitor deficiencies (acquired or inherited). An additional indication is to monitor patients on complement-regulating drugs, an indication which may be expected to increase in the near future since there is now a number of such drugs either under development, already in clinical trials or in clinical use. Available techniques to study complement include quantification of: (1) individual components; (2) activation products, (3) function, and (4) autoantibodies to complement proteins. In this review, we summarize the appropriate indications, techniques, and interpretations of basic serological complement analyses, exemplified by a number of clinical disorders.

  • 5.
    Persson, Barbro
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Englund,
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Saxner, A. Joelsson
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Säfwenberg, Jan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    A Follow-Up Study of RhD neg Patients Deliberately Receiving RhD pos Red Cell Units2013In: Transfusion, ISSN 0041-1132, E-ISSN 1537-2995, Vol. 53, p. 151A-151AArticle in journal (Other academic)
  • 6.
    Persson, Barbro
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    McAree, Fionnuala
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Muller, Malin
    Trollmo, Tina
    Parodis, Ioannis
    Jonsdottir, Thorunn
    Malmstrom, Vivianne
    Gunnarsson, Iva
    Rönnelid, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Disappearance and Reappearance of IgG, IgA and IgM Autoantibody Isotypes and Immune Complexes in Rituximab-Treated SLE Patient2013In: Annals of the Rheumatic Diseases, ISSN 0003-4967, E-ISSN 1468-2060, Vol. 72, p. A34-A34Article in journal (Other academic)
    Abstract [en]

    Background and Objectives We have earlier investigated the content of specific IgG autoantibodies in SLE immune complexes (IC; Åhlin et al, Lupus 2012; 21:586). For that purpose we have developed a line blot technique for the quantification also of non-classical (IgA and IgM) SLE autoantibody isotypes. In SLE patients, IgG autoantibody levels drop after institution of Rituximab therapy. The objective was to investigate parallel changes IgG, IgA and IgM autoantibody isotypes in parallel to IC levels.

    Materials and Methods Nine SLE patients initially treated with two infusions of Rituximab were followed with repeated samplings at baseline and after 1, 3, 6 and 12 months. Thawed samples were investigated simultaneously concerning rheumatoid factor (RF) isotypes and C1q-binding IC with enzyme immunoassays. All samples from patients with ANA-associated autoantibodies (6/9) were investigated concerning IgG/A/M autoantibodies with line blot quantitated with densitometry and concerning IgG autoantibodies with ALBIA/Luminex technique. Significant changes were defined either as ≥33% drop or as ≥50% increase, compared to the lowest levels experienced during the follow-up period.

    Results ALBIA measurements showed significant initial drop in anti-dsDNA in 4/6 patients but also significant drop in levels of anti-histone, anti-SSA/Ro60, anti-Sm and anti-Sm/RNP in individual patients. Late increases in IC and antibodies against dsDNA, SSA/Ro52, SSA/Ro60, SSB, Sm, Sm/RNP ribosomal P protein and histones were associated with clinical relapse. Late increase in IgA/IgM anti-DNA, anti-histones and anti-nucleosomes was also found in one patient with persistent kidney disease treated with mycophenolate mofetil at 10 months. Non-classical autoantibody isotypes showed late increases that often were not paralleled by the corresponding IgG autoantibodies. Two patients showed late increase in RF isotypes in parallel to clinical relapse. Different autoantibodies/isotypes showed different kinetics of appearance/disappearance. All ANA autoantibody positive patients initially had increased IC levels, which dropped significantly after therapy in 4/6 patients. The autoantibody negative patients never had increased IC levels and showed no significant changes in RF.

    Conclusions Measurement of non-classical isotypes of RF and ANA-associated autoantibodies might yield clinically useful information when monitoring SLE patients treated with B cell depleting therapy.

  • 7.
    Sandholm, Kerstin
    et al.
    Linnaeus Univ, Linnaeus Ctr Biomat Chem, Kalmar, Sweden.
    Persson, Barbro
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Skattum, Lillemor
    Lund Univ, Sect Microbiol, Dept Lab Med Immunol & Glycobiol, Lund, Sweden.
    Eggertsen, Gosta
    Karolinska Inst, Dept Lab Med, Stockholm, Sweden;Karolinska Univ Lab, Clin Chem, Stockholm, Sweden.
    Nyman, Dag
    Aland Cent Hosp, Aland Borrelia Grp, Mariehamn, Finland.
    Gunnarsson, Iva
    Karolinska Inst, Karolinska Univ Hosp, Dept Med, Rheumatol Unit, Stockholm, Sweden.
    Svenungson, Elisabet
    Karolinska Inst, Karolinska Univ Hosp, Dept Med, Rheumatol Unit, Stockholm, Sweden.
    Nilsson, Bo
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Nilsson Ekdahl, Kristina
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology. Linnaeus Univ, Linnaeus Ctr Biomat Chem, Kalmar, Sweden.
    Evaluation of a Novel Immunoassay for Quantification of C1q for Clinical Diagnostic Use2019In: Frontiers in Immunology, ISSN 1664-3224, E-ISSN 1664-3224, Vol. 10, article id 7Article in journal (Refereed)
    Abstract [en]

    Objectives: C1q is a valuable biomarker of disease activity in systemic lupus erythematosus (SLE). The "gold standard" assay, rocket immunoelectrophoresis (RIE), is time-consuming, and thus a shift to soluble immune precipitation techniques such as nephelometry has occurred. However, quantification of C1q with these techniques has been questioned as a result of the antibody binding properties of C1q. In the present work, we have compared results using various techniques (RIE, nephelometry, and ELISA) and have developed and validated a new magnetic bead-based sandwich immunoassay (MBSI). Methods: C1q was quantified by nephelometry and the new sandwich immunoassay in 45 serum samples analyzed using RIE. C1q was also assessed in plasma using RIE and sandwich immunoassay in samples from SLE patients with nephritis (n = 69), SLE patients without nephritis (n = 310) as classified by BILAG score, and matched controls (n = 322). In addition, cerebrospinal fluid (CSF) samples from 31 patients, previously analyzed with ELISA, were also analyzed with the MBSI to test the behavior of this new assay in the lower detection range. Results: We found a strong correlation between the new MBSI, RIE, and ELISA, but not with nephelometry. The MBSI demonstrated lower levels of C1q in SLE patients than in matched controls (p < 0.0001), and patients with nephritis had lower levels than patients without nephritis (p < 0.01). Similarily, RIE showed significant differences between the patient groups (p < 0.0001). An association was also found between the levels of C1q and the SLE disease activity index (SLEDAI). Furthermore, there was good correlation between the values obtained by MBSI and ELISA, in both serum (r = 0.960) and CSF (r = 0.786), underscoring the ability of both techniques to measure low concentrations of C1q with high accuracy. Conclusion: The sandwich immunoassay correlated well with RIE, but soluble immune precipitation techniques, such as nephelometry, did not appear suitable alternatives, since C1q itself, and possibly anti-C1q antibodies, interfered with the measurements. The new sandwich immunoassay is therefore a good replacement for RIE in monitoring SLE disease activity.

  • 8.
    Westman, Gabriel
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Infectious Diseases.
    Studahl, Marie
    Department of Infectious Diseases, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden.
    Persson, Barbro
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Ahlm, C.
    Umea Univ, Dept Clin Microbiol, Infect Dis, Umea, Sweden.
    Eriksson, Britt-Marie
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Infectious Diseases.
    Rönnelid, Johan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Clinical Immunology.
    Schliamser, Silvia
    Department of Clinical Sciences, Lund University, Lund, Sweden.
    Aurelius, Elisabeth
    Unit of Infectious Diseases, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Sweden.
    N-Methyl-D-Aspartate Receptor Autoimmunity Affects Cognitive Performance in Herpes Simplex Encephalitis2016In: Clinical Microbiology And Infection, ISSN 1198-743X, Vol. 22, no 11, p. 934-940Article in journal (Refereed)
    Abstract [en]

    Objectives: To investigate the prevalence and temporal development of N-methyl-D-aspartate receptor (NMDAR) autoantibodies in relation to neurocognitive performance in patients with herpes simplex encephalitis (HSE). Methods: This prospective observational study enrolled a total of 49 HSE patients within a randomized controlled trial of valacyclovir. Cerebrospinal fluid and serum samples were drawn in the initial stage of disease, after 2 to 3 weeks and after 3 months. Anti-NMDAR IgG was detected with HEK293 cells transfected with plasmids encoding the NMDA NR1 type glutamate receptor. A batch of neurocognitive tests, including the Mattis Dementia Rating Scale (MDRS), Glasgow Coma Scale (GCS), Reaction Level Scale (RLS85), Mini-Mental State Examination (MMSE) and National Institutes of Health (NIH) stroke scale, was performed during 24 months' follow-up. Results: Anti-NMDAR IgG was detected in 12 of 49 participants. None were antibody positive in the initial stage of disease. In ten of 12 positive cases, specific antibodies were detectable only after 3 months. Notably, the development of NMDAR autoantibodies was associated with significantly impaired recovery of neurocognitive performance. After 24 months' follow-up, the median increase in MDRS total score was 1.5 vs. 10 points in antibody-positive and -negative participants (p = 0.018). Conclusions: Anti-NMDAR autoimmunity is a common complication to HSE that develops within 3 months after onset of disease. The association to impaired neurocognitive recovery could have therapeutical implications, as central nervous system autoimmunity is potentially responsive to immunotherapy.

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