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Strategies for Immunointerventions in Dermatology pp 227–241Cite as

Rheumatic Disease Group

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Abstract

In the recent past, advances in both basic and clinical research have considerably contributed to our understanding of the cellular and molecular events that lead to autoimmune disease. The importance of genetic susceptibility [1], i.e., particular alleles of major histocompatibility complex (MHC) class II molecules [2], and environmental factors, i.e., molecular mimicry of autoantigens by microbes [3] and microbial super- antigens [4], as well as the central role of T cells [5] in the pathogenesis of autoimmune disease is well appreciated, and modern immune-based therapy would thus ideally be directed towards early events in the pathological process. Results obtained using animal models of antigen-induced autoimmune disease, e.g., collagen-induced arthritis and experimental allergic encephalomyelitis, have resulted in optimism that this will eventually be possible. It must be borne in mind, however, that in this type of experimental animal model it is simple to intervene in the development of autoimmune disease, since the induction events (immunization with defined autoantigens) are designed by the investigator. In contrast, in autoimmune disorders of the rheumatic disease group, including lupus erythematosus (LE) systemic sclerosis, dermatomyositis (DM), and polyarteritis nodosa (PAN), we do not know whether a specific autoantigen initiated the disease, nor do we know the time point at which the antigenic challenge occurred. The processes resulting in autoimmune disease begin well before we see the patient, and we as clinicians are faced only with late-term manifestations of the immunologic events that lead to clinical disease. Thus the current therapy of these diseases is essentially limited to chemical immunosuppresssion with corticosteroids and cvtotoxic drugs, such as azathioprine, cyclophosphamide, and methotrexate. The introduction of cyclosporin represents major progress compared with substances formerly used in terms of cellular selectivity, inasmuch as cyclosporine does not depress bone marrow hemopoesis and acts selectively on the production of well-defined cytokines [6]. However, significant side effects occur, and the lymphokines in question are involved in a number of immune reactions other than the targeted process [7].

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  1. R. M. Trüeb
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Editors and Affiliations

  1. Department of Dermatology, University Hospital Zurich, Gloriastrasse 31, CH-8091, Zurich, Switzerland

    Günter Burg M.D. (Chairman) (Chairman)

  2. Department of Dermatology, University Hospital Zurich, Gloriastrasse 31, CH-8091, Zurich, Switzerland

    Reinhard G. Dummer M.D.

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Trüeb, R.M. (1997). Rheumatic Disease Group. In: Burg, G., Dummer, R.G. (eds) Strategies for Immunointerventions in Dermatology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60752-3_20

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