Humoral autoimmunity as a mediator of CNS repair |
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| Affiliation: | 1. Rheumatology Fellowship and Training Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA;2. Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA;1. Laboratory of Immune Regulation, Immunology Frontier Research Center, Osaka University, Osaka 565 0871, Japan;2. Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur 342005, India;3. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA;1. Department of Chemistry, Imperial College London, Molecular Sciences Research Hub, London W12 0BZ, UK;2. The Francis Crick Institute, London NW1 1AT, UK |
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| Abstract: | Autoimmune responses directed against the central nervous system (CNS) have generally been considered pathogenic in nature. Although there are several well understood conditions in which this is the case, there is also a growing body of experimental evidence to show that both the cellular and humoral immune responses can promote tissue repair following CNS injury and disease. Our laboratory has used a mouse model of chronic demyelinating disease to characterize a class of polyreactive IgM autoantibodies that react with oligodendrocyte surface antigens and promote myelin repair. By screening a large number of human monoclonal antibodies, we have found that IgM antibodies that react with CNS tissue are relatively common. Autoreactive IgM antibodies might constitute an endogenous system for tissue repair, and therefore these antibodies could be of value as therapeutic reagents. |
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