Interleukin 2 deficiencies in rheumatoid arthritis and systemic lupus erythematosus

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Abstract

The ability of peripheral blood lymphocytes from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and Sjogren's syndrome (SS) to produce interleukin 2 (IL-2) and respond to it in-vitro was examined. Phytohemagglutinin-stimulated lymphocytes from over half of the SLE patients exhibited a decreased ability to produce IL-2 while their concanavalin A-generated blast cells responded normally to exogenous IL-2. Lymphocytes from RA patients not only produced less IL-2 than normals (P < 0.001), but also responded poorly to exogenous IL-2 (P = 0.011). These abnormalities did not correlate with the patient's age, sex, duration of disease, or disease activity. Production of and response to IL-2 was widely varied among patients with SS and not different from controls. The decreased response of RA lymphocytes to IL-2 may result from a smaller number of cell surface IL-2 receptors since IL-2 adsorption to RA cells was lower than to either SLE or normal cells. These data suggest that IL-2-related abnormalities may play a role in the disordered immunoregulation characteristic of RA and perhaps of SLE.

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