Several aspects of interleukin-2 (IL-2) generation and function were studied employing mononuclear cells from synovial fluid (SF), synovial tissue (ST) and peripheral blood (PB) of patients with rheumatoid arthritis (RA). Decreased PHA stimulated IL-2 production by lymphocytes from rheumatoid ST, SF (P < 0.02), and PB (P < 0.01) was observed when compared to normal blood and SF of patients with gout. The proliferative response of rheumatoid lymphocyte blasts exposed to exogenous IL-2 was also defective (P < 0.05-0.001). This defect was greater in SF than in rheumatoid PB (P < 0.05-0.001). In addition to the proliferative response, the effect of IL-2 on interferon-gamma (IFN-γ) production was also examined. Rheumatoid lymphocytes from both PB and SF produced less IFN-γ after overnight treatment with IL-2 than did normal PB lymphocytes. This decreased IFN-γ induction was discordant with the excellent enhancement by IL-2 of natural killer activity. Removal of adherent cells in synovial fluid did not correct this deficit. Abnormalities in the biology of IL-2 and IFN-γ suggest that impaired T cell function could contribute to the immunopathogenesis of RA.
|Original language||English (US)|
|Number of pages||9|
|Journal||Clinical and Experimental Immunology|
|State||Published - Apr 24 1985|
ASJC Scopus subject areas
- Immunology and Allergy