Abnormalities of t cell activation in the rheumatoid synovium detected with monoclonal antibodies to CD3

N. Talal, Z. Tovar, M. J. Dauphinee, E. Flescher, H. Dang, D. Galarza

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


The chronic inflammation of rheumatoid arthritis (RA) is associated with hypofunction of synovial fluid (SF) T cells. We studied the mechanisms leading to this abnormality using a mitogenic monoclonal antibody specific for the T cell receptor-associated CD3 complex. We found that SF cells are defective in their response to anti-CD3 antibodies as measured by proliferation, generation of natural cytotoxicity, and induction of the Tac (p55) component of the IL2 receptor. Nevertheless, these cells do bear functional IL2 receptors and are more responsive to IL2 than are resting peripheral blood T cells. In searching for a mechanism to explain the reduced IL2 production, we found that polyamines (whose oxidation products can down-regulate proliferation and IL2 production) are elevated in RA cells from both blood and SE We postulate that the chronic activation of RA T cells triggers this feedback loop which constitutes a defensive mechanism aimed at reducing the T cell driven autoimmune and inflammatory process.

Original languageEnglish (US)
Pages (from-to)175-182
Number of pages8
JournalScandinavian Journal of Rheumatology
Issue numberS76
StatePublished - 1988


  • IL2 receptor
  • Monoclonal antibodies to CD3
  • Natural killing
  • Polyamines
  • T cell hyporesponse in RASF

ASJC Scopus subject areas

  • Immunology and Allergy
  • Rheumatology
  • Immunology


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