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  • 1. Halminen, M
    et al.
    Juhela, S
    Vaarala, Outi
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Pediatrics. Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Barn.
    Simell, O
    Induction of interferon-gamma and IL-4 production by mitogen and specific antigens in peripheral blood lymphocytes of Type 1 diabetes patients.2001In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 34Article in journal (Refereed)
  • 2.
    Hultgren, O
    et al.
    Klin Immunol Göteborg.
    Hahn-Zoric, M
    Klin Immunol Göteborg.
    Andersson, B
    Klin Immunol Göteborg.
    Almroth, Gabriel
    Linköping University, Department of Medical and Health Sciences, Nephrology. Linköping University, Faculty of Health Sciences.
    Serum concentration of interleukin-18 is up-regulated in patients with ANCA-associated vasculitis2007In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 40, no 7, p. 529-531Article in journal (Refereed)
    Abstract [en]

    We investigated circulating interleukin-18 concentrations in patients with ANCA-associated vasculitis (ASV) and healthy control subjects, and included a group of hemodialysis patients, a patient group previously reported to show high IL-18 plasma levels. Anti-proteinase 3 (PR3) and anti-myeloperoxidase (MPO) serum levels were also measured. Interestingly we found significantly increased serum IL-18 concentrations in ASV patients as compared to healthy controls, 437 vs. 185 pg/ml (p < 0.0001). The increase of IL-18 production was similar irrespective of presence of autoantibodies to PR3 or MPO. As expected the hemodialysis patients also showed significantly increased circulating IL-18 concentrations as compared to control subjects.

  • 3. Landin-Olsson, M
    et al.
    Arnqvist, Hans
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Blohmé, G
    Littorin, B
    Lithner, F
    Nyström, L
    Scherstén, B
    Sundkvist, G
    Wibell, L
    Östman, J
    Lernmark, Å
    Appearance of islet cell autoantibodies after clinical diagnosis of diabetes mellitus.1999In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 29, p. 57-63Article in journal (Refereed)
  • 4.
    Sjöwall, Christoffer
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Rheumatology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Rheumatology.
    Olin, Anders I.
    Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden.
    Skogh, Thomas
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Rheumatology.
    Wetterö, Jonas
    Linköping University, Department of Clinical and Experimental Medicine, Division of Inflammation Medicine. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Heart and Medicine Center, Department of Rheumatology.
    Mörgelin, Matthias
    Infection Medicine, Department of Clinical Sciences, Lund University, Lund, Sweden.
    Nived, Ola
    Rheumatology, Department of Clinical Sciences, Lund University, Lund, Sweden.
    Sturfelt, Gunnar
    Rheumatology, Department of Clinical Sciences, Lund University, Lund, Sweden.
    Bengtsson, Anders A.
    Rheumatology, Department of Clinical Sciences, Lund University, Lund, Sweden.
    C-reactive protein, immunoglobulin G and complement co-localize in renal immune deposits of proliferative lupus nephritis2013In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 46, no 3, p. 205-214Article in journal (Refereed)
    Abstract [en]

    The pattern recognition molecules C-reactive protein (CRP) and C1q are of big interest in relation to the pathogenesis of systemic lupus erythematosus (SLE). Circulating autoantibodies against CRP and C1q are frequently found in SLE patients with active disease, particularly in lupus nephritis (LN), and rising levels reportedly relate to disease activity and outcome. If CRP-, or dsDNA- and/or C1q-containing immune complexes (ICs) are pathogenic in LN, glomerular IgG-deposits would be expected to co-localize with these antigens. In search for proof of this concept, renal biospsies from patients with active LN (n=5) were examined with high-resolution immunogold electron microscopy. Renal biopsies from patients with Henoch-Schönlein purpura, pauci-immune nephritis and renal cancer served as controls. IgG antibodies against CRP, C1q and nucleosomes were analyzed in pre–post flare sera. We could demonstrate that CRP, C1q, C3c and dsDNA were co-localized with IgG in electron dense deposits in the glomerular basement membrane/subendothelial space in all of the 5 LN patients. Deposits of IgG, CRP, complement and dsDNA were 10-fold higher in LN compared to controls. All SLE patients had circulating anti-nucleosome antibodies; 4/5 had serum antibodies against CRP, dsDNA, and C1q at biopsy/flare. Despite a limited number of cases, the results support the notion of a pathogenic role not only for anti-dsDNA antibodies, but also for anti-CRP and anti-C1q in LN. The glomerular ICs may have been generated by deposition of circulating ICs or by in situ IC formation.

  • 5.
    Stechova, Katerina
    et al.
    Dept of Pediatrics Prague.
    Kolouskova, Stanislava
    Dept of Pediatrics Prague.
    Sumnik, Zdenek
    Dept of Pediatrics Prague.
    Cinek, Ondrej
    Dept of Pediatrics Prague.
    Kverka, Milosav
    The Inst of Microbiology Prague.
    Faresjö, Maria
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Pediatrics.
    Chudoba, Daniel
    Dept of Biology and Genetics Prague.
    Dovolilova, Eva
    Diabetes Centrum Prague.
    Pechova, Marta
    Dept of Biochemistry Prague.
    Vrabelova, Zuzana
    Dept of Pediatrics Prague.
    Böhmova, Kristyna
    Dept of Pediatrics Prague.
    Janecek, Lukas
    Dept of Pediatrics Prague.
    Saudek, Frantisek
    Diabetes Centrum Prague.
    Vavrinec, Jan
    Dept of Pediatrics Prague.
    Anti-GAD65 reactive peripheral blood mononuclear cells in the pathogenesis of cystic fibrosis related diabetes mellitus2005In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 38, no 4, p. 319-323Article in journal (Refereed)
    Abstract [en]

    Objective: A role of autoreactive T cells for type 1 diabetes pathogenesis is considered crucial. In our pilot study we addressed if autoreactive mononuclear cells are present also in peripheral blood of patients with other specific forms of diabetes as cystic fibrosis related diabetes (CFRD). Methods: Cellular immune responses to a known β-cell autoantigen (GAD65 and GAD65 derived peptides) were analysed by ELISPOT (IFN-γ) and by protein microarray analysis in four patients suffering from CFRD, in four cystic fibrosis (CF) patients without diabetes, in eight type 1 diabetes patients (without CF) and in four healthy controls. Results: Response to the autoantigen GAD65 (protein and peptides) was observed in 7/8 patients suffering from CF and in all type 1 diabetes patients. Post-stimulation production of Th1 cytokines (IFN-γ, TNF-β) was observed in 2/4 CFRD, 1/4 CF patients and in 7/8 type 1 diabetes patients. All these patients carry prodiabetogenic HLA-DQ genotype. Th2- and Th3 type of cytokine pattern was observed in 2/4 CF patients. Production of IL-8 was observed in the third CFRD as well as in the third CF patient and in 1/8 type 1 diabetes patient and borderline production of this chemokine was also observed in 2/4 healthy controls. No reaction was observed in the other 2/4 healthy controls and in the fourth CFRD patient who carried a strongly protective genotype and did not produce autoantibodies. The most potent peptide of GAD65 was amino acids 509-528. Conclusions: We consider our observations as a sign of a reaction directed against the self-antigen GAD65 that are closely connected to type 1 diabetes. In CF patients who do not develop diabetes autoreactive mechanisms are very probably efficiently suppressed by immune self-tolerance mechanisms. CFRD patients are a heterogenic group. To disclose those who may display features of autoimmune diabetes could have an impact for their therapy and prognosis. © 2005 Taylor & Francis Group Ltd.

  • 6.
    Tiittanen, Minna
    et al.
    Avd för Molekylär Medicin Helsingfors, Finland.
    Knip, Mikael
    Barn och Ungdomssjukhuset Helsingfors, Finland.
    Vaarala, Outi
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Pediatrics. Östergötlands Läns Landsting, Centre of Paediatrics and Gynecology and Obstetrics, Department of Paediatrics in Linköping.
    Anti-insulin activity in IgG-fractions from children with newly-diagnosed type 1 diabetes and negative for insulin autoantibodies2004In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 37, no 1, p. 45-49Article in journal (Refereed)
    Abstract [en]

    Insulin autoantibodies (IAA) are often detected as the first humoral sign of β-cell autoimmunity in prospective studies in young children with increased genetic risk of type 1 diabetes. After the appearance of IAA their level typically rise but seems to decline in many cases before the clinical presentation of type 1 diabetes. We hypothesized that the reason for the sudden drops in the levels of IAA could be the formation of immune complexes caused by binding of antibodies to free insulin in plasma. We studied whether isolation of the IgG-fraction and dissociation of immune complexes by acid treatment using protein A column results in the appearance of detectable IAA in those children with newly-diagnosed type 1 diabetes whose plasma samples test negative for IAA. IAA assay was performed in IgG-fractions and corresponding plasma samples from 17 children with type 1 diabetes and 23 unaffected children all testing negative for plasma IAA. The levels of IAA measured from IgG-fractions of diabetic children were higher than the levels of IAA measured from IgG-fractions in the control children (p = 0.004 in Mann-Whitney U-test). Forty-seven percent (8 out of 17) of newly-diagnosed patients negative for plasma IAA before IgG separation had increased levels of IAA in IgG-fractions and only 13% (3 out of 23) of controls. The levels of glutamate decarboxylase autoantibodies (GADA) did not differ between patients (n = 14) and controls (n = 21) negative for plasma GADA when measured in IgG-fractions. Our results suggest that formation of immune complexes results in false negative results in tests for IAA but not for GADA.

  • 7. Törn, C
    et al.
    Landin-Olsson, M
    Lernmark, Å
    Scherstén, B
    Östman, J
    Arnqvist, Hans
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology. Östergötlands Läns Landsting, MKC-2, GE: endomed.
    Björk, E
    Blohmé, G
    Bolinder, J
    Eriksson, J
    Littorin, B
    Nyström, L
    Sundkvist, G
    Combinations of beta cell specific autoantibodies at diagnosis of diabetes in young adults reflects different courses of beta cell damage.2001In: Autoimmunity, ISSN 0891-6934, E-ISSN 1607-842X, Vol. 33, p. 115-120Article in journal (Refereed)
1 - 7 of 7
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