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From immunohistochemistry to pathophysiology of rheumatoid arthritis: cross reactivity of self anti-immunoglobulin antibodies with collagen(s) may contribute to mechanisms of connective tissue damage (a hypothesis).

The mechanism of initiation and development of rheumatoid arthritis was a subject of several hypotheses. None of those hypotheses has, however, convincingly explained all important facts, related to clinical, immunological and pathological aspects of the disease. A hypothesis is presented here, suggesting that, in the course of rheumatoid arthritis, an immune system produces anti-immunoglobulin antibodies, cross-reacting with self collagen(s). This cross-reactivity may be a significant part of the complex set of pathological phenomena, characteristic for rheumatoid arthritis. The hypothesis originated from the author's own observations of binding of the anti-immunoglobulin antibodies to the fibrous connective tissue (presumably to collagens contained in it) in histological sections, subjected to immunohistochemical procedures.