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.
Rowiński
Jan
J
Department of Anatomy, Faculty of Physical Education in Biała Podlaska, Poland. jan.rowinski@awf-bp.edu.pl
D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology; D001323:Autoantibodies / Q000032:analysis*; D003094:Collagen / Q000276:immunology*; D003238:Connective Tissue / Q000276:immunology / Q000473:pathology*; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D018448:Models, Immunological
D001323:Autoantibodies; D007074:Immunoglobulin G; D003094:Collagen