Cytokines and the chronic inflammation of rheumatic disease. III. Deficient interleukin-2 production in rheumatoid arthritis is not due to suppressor mechanisms.
Despite the evidence for activated T cells in the joint in rheumatoid arthritis (RA), there is evidence of deficient lymphocyte proliferation to a variety of stimulants. We investigated the production of interleukin-2 (IL-2) after phytohemagglutinin (PHA) stimulation. We show that in the peripheral blood IL-2 production was similar in RA and controls (3.7 vs 3.0 U/ml, respectively). However, blood lymphocytes from patients with joint effusions produced significantly less IL-2 than from patients without effusions (1.8 vs 5.7 U/ml, respectively). The amount of IL-2 produced by synovial fluids (SF) cells was significantly less than that produced by the corresponding blood cells (1.0 vs 1.6 U/ml). Further experiments revealed that the decreased IL-2 production was not due to its removal by IL-2 receptor positive cells in the SF and cell mixing experiments did not reveal any suppressor influences.
D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000276:immunology*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D007376:Interleukin-2 / Q000096:biosynthesis*; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D011971:Receptors, Immunologic / Q000276:immunology; D015375:Receptors, Interleukin-2; D013582:Synovial Fluid / Q000276:immunology; D013583:Synovial Membrane / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
D007376:Interleukin-2; D011971:Receptors, Immunologic; D015375:Receptors, Interleukin-2