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Immunopathogenetic mechanisms of arthritis and modes of action of antirheumatic therapies

  • A. C. Allison

Abstract

The aetiology of rheumatoid arthritis (RA) remains unknown. There is no evidence for bacterial involvement, which is the case in rheumatic fever, Lyme arthritis and Reiter’s disease. Although acute viral infections such as rubella can produce arthritis, there is no evidence that rubella or any other virus is specifically associated with RA. While responses of lymphocytes from RA patients to Epstein-Barr virus have provided interesting information1, no causal relationship has been established. The pattern of disease, and responses to immunosuppressive drugs, leave little doubt that immune reactions to an exogenous agent or agents, or to host components, are involved. In other words, the pathogenesis of RA is an immunologically driven, chronic inflammatory reaction. There are certainly autoimmune manifestations in RA, notably production of antiglobulins or rheumatoid factors; but the aetiology of autoimmunity is itself obscure and likely to be due to complex interactions of host genetic and environmental factors2,3. Whether rheumatoid factors play a causal role in RA is an unresolved question, which will be discussed below.

Keywords

Rheumatoid Arthritis Major Histocompatibility Complex Synovial Fluid Rheumatoid Factor Rheumatoid Arthritis Synovia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© MTP Press Limited 1988

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  • A. C. Allison

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