Pathogenesis of rheumatoid arthritis.

Abstract:

:Rheumatoid arthritis (RA) is initiated by an unknown antigen(s) in the genetically programmed host. HLA-DR4 is associated with RA. The antigen could be exogenous (e.g., Epstein-Barr virus, bacterial cell wall products) or endogenous (e.g., collagen or immunoglobulin). Within the synovium, where the immune response begins, monocytes and lymphocytes are activated. Polyclonal B-cell proliferation results, as well as production of monokines and lymphokines. The antibodies form immune complexes with other antibody molecules or antigens. Phagocytosis of immune complexes results in production of many autacoids and activation of other soluble mediator systems, e.g., the coagulation, kinin, complement, and fibrinolytic systems in synovial fluid. Chemotactic factors draw polymorphonuclear leukocytes into the joint space. Monokines stimulate synovial cell proliferation; these cells, in turn, synthesize proteinases and products of arachidonate metabolism capable of destroying normal articular structures.

journal_name

Clin Orthop Relat Res

authors

Harris ED Jr

subject

Has Abstract

pub_date

1984-01-01 00:00:00

pages

14-23

issue

182

eissn

0009-921X

issn

1528-1132

pub_type

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