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University of Toronto, Ontario, Canada.
The infectious etiology of rheumatoid arthritis has been a long-standing hypothesis and in recent years is being examined with greater sophistication and scientific rigor. Synovitis may result indirectly from infection by the deposition of circulating immune complexes, by molecular mimicry, by in situ antigen deposition, or by arthritogenic toxins. Of candidate pathogens, recent interest has focused on mycobacterial HSP, EBV, and parvovirus B19. There is circumstantial evidence to support a link between each of these microorganisms and RA but presently all fall short of definitive proof of causality. It is anticipated that clearer answers may be forthcoming on this perplexing and intriguing question with the application of molecular biologic techniques to the study of synovial tissues.
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