Characterization of the defective autologous mixed lymphocyte response in rheumatoid arthritis.
In order to characterize the autologous mixed lymphocyte response (AMLR) in patients with rheumatoid arthritis (RA) and to define the relationship with disease activity, peripheral blood T lymphocytes were stimulated with either a B lymphocyte-enriched (B cells) or a macrophage-enriched (macrophages) population. A significant reduction (P less than 0.01 to P less than 0.001) of T cell proliferation stimulated both by B cells and macrophages was observed in patients with active disease. The B lymphocytes were significantly less stimulatory (P less than 0.02 to P less than 0.001) than macrophages in the patients compared with the controls. In the normal controls, macrophages in higher concentrations were capable of suppressing the B lymphocyte-stimulated AMLR, but macrophages from patients with RA were not excessively suppressive. A significant association (P less than 0.02) was observed between disease activity and the AMLR. Using the B-enriched population, the AMLR proliferative response was significantly associated (P less than 0.001) with the production of interleukin-2. Defects in proliferation could only be partially restored by the addition of interleukin-2. These data indicate that the defective AMLR observed in patients with RA is related to disease activity and is associated with altered cellular interactions among T lymphocytes, macrophages, and the B lymphocyte-enriched population.
D001172:Arthritis, Rheumatoid / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D002450:Cell Communication; D006801:Humans; D007376:Interleukin-2 / Q000096:biosynthesis; D008213:Lymphocyte Activation; D007959:Lymphocyte Culture Test, Mixed; D008264:Macrophages / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D013997:Time Factors
D007376:Interleukin-2