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  • 1.
    Forsman, Huamei
    et al.
    University of Gothenburg.
    Islander, Ulrika
    University of Gothenburg.
    Andréasson, Emil
    University of Gothenburg.
    Andersson, Annica
    University of Gothenburg.
    Önnheim, Karin
    University of Gothenburg.
    Karlström, Alexandra
    University of Gothenburg.
    Sävman, Karin
    University of Gothenburg.
    Magnusson, Mattias
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Medical Immunology.
    Brown, Kelly L
    University of Gothenburg.
    Karlsson, Anna
    University of Gothenburg.
    Galectin 3 Aggravates Joint Inflammation and Destruction in Antigen-Induced Arthritis2011In: ARTHRITIS AND RHEUMATISM, ISSN 0004-3591, Vol. 63, no 2, p. 445-454Article in journal (Refereed)
    Abstract [en]

    Objective. Galectin 3, an endogenous beta galactoside-binding lectin, plays an important role in the modulation of immune responses. The finding that galectin 3 is present in the inflamed synovium in patients with rheumatoid arthritis suggests that the protein is associated with the pathogenesis of this disease. We undertook this study to investigate the influence of galectin 3 deficiency in a murine model of arthritis. Methods. Wild-type (WT) and galectin 3-deficient (galectin 3(-/-)) mice were subjected to antigen-induced arthritis (AIA) through immunization with methylated bovine serum albumin. The concentration of serum cytokines (interleukin-6 [IL-6] and tumor necrosis factor alpha [TNF alpha]) and antigen-specific antibodies was evaluated using a cytometric bead array platform and enzyme-linked immunosorbent assay (ELISA). Cellular IL-17 responses were examined by flow cytometry, ELISA, and enzyme-linked immunospot assay. Results. The joint inflammation and bone erosion of AIA were markedly suppressed in galectin 3(-/-) mice as compared with WT mice. The reduced arthritis in galectin 3(-/-) mice was accompanied by decreased levels of antigen-specific IgG and proinflammatory cytokines. The frequency of IL-17-producing cells in the spleen was reduced in galectin 3(-/-) mice as compared with WT mice. Exogenously added recombinant galectin 3 could partially restore the reduced arthritis and cytokines in galectin 3(-/-) mice. Conclusion. Our findings show that galectin 3 plays a pathogenic role in the development and progression of AIA and that the disease severity is accompanied by alterations of antigen-specific IgG levels, systemic levels of TNF alpha and IL-6, and frequency of IL-17-producing T cells. To our knowledge, this is the first report of in vivo evidence that galectin 3 plays a crucial role in the development of arthritis.

  • 2.
    Magnusson, Mattias
    Linköping University, Department of Clinical and Experimental Medicine, Medical Immunology. Linköping University, Faculty of Health Sciences.
    Typ I IFN skyddar mot antigeninducerad artrit2011In: Best Practice, Vol. 7, p. 12-14Article in journal (Other academic)
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