Cytokines and the chronic inflammation of rheumatic disease. III. Deficient interleukin-2 production in rheumatoid arthritis is not due to suppressor mechanisms

J Rheumatol. 1987 Oct;14(5):902-6.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Arthritis, Rheumatoid / immunology*
  • Female
  • Humans
  • In Vitro Techniques
  • Interleukin-2 / biosynthesis*
  • Lymphocyte Activation
  • Male
  • Middle Aged
  • Receptors, Immunologic / immunology
  • Receptors, Interleukin-2
  • Synovial Fluid / immunology
  • Synovial Membrane / immunology
  • T-Lymphocytes, Regulatory / immunology*

Substances

  • Interleukin-2
  • Receptors, Immunologic
  • Receptors, Interleukin-2