Abstract

Purified blood monocytes from patients with rheumatoid arthritis released enhanced amounts of the arachidonic acid products PGE, TXB 2, and 6-keto-PGF α when compared to monocytes from healthy control individuals. The proliferative response of blood lymphocytes to concanavalin A was strongly suppressed in rheumatoid arthritis patients. Suppression of lymphocyte proliferation could not be reversed by in vitro addition of indomethacin, an inhibitor of prostaglandin synthesis. However, a restoration of lymphocyte proliferation was possible by reducing the high percentage of monocytes in the mononuclear cell fraction of rheumatoid arthritis patients (50 ± 6% versus 23 ± 5% in healthy controls). Although these findings indicate that monocytes of rheumatoid arthritis patients display a “stimulated” arachidonic acid metabolism, the depressed lymphocyte response appears to be due to the high number of monocytes and not to an enhanced PGE release.

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