Abstract
Autoimmune diseases are thought to result from a dysregulation of the immune system leading to loss of self-tolerance and autoaggression via antigen-specific T and B cell responses. Whether or not these responses are directed against true autoantigens or cross-reacting epitopes of microbial origin remains a matter of intense debate and research (Schwimmbeck et al. 1987; Steglitz et al. 1989; Hermann 1991; Smiley and Hoffmann 1991; Kaufmann 1990). Nevertheless, an ever-increasing number of high-titer autoantibodies of the IgG and IgA isotypes are being reported (Brostoff et al. 1991; Pisetzky 1991). Most of these autoantibodies are associated with distinct clinicopathologic conditions. Thus, various types of antinuclear antibodies (ANA) are specific markers of certain collagen vascular diseases, antimitochondrial antibodies (ANA) are associated with autoimmune liver disease and antineutrophil cytoplasmic autoantibodies (ANA) with necrotizing granulomatous vasculitis or crescentic glomerulonephritis (Jennette and Falk 1992).
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Peter, H.H. (1993). Current Principles and Perspectives in the Treatment of Autoimmune Disease. In: Eibl, M.M., Huber, C., Peter, H.H., Wahn, U. (eds) Symposium in Immunology I and II. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-78087-5_18
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DOI: https://doi.org/10.1007/978-3-642-78087-5_18
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