Suppression and prevention of adjuvant arthritis in rats by a monoclonal antibody to the alpha/beta T cell receptor

Eur J Immunol. 1990 Dec;20(12):2805-8. doi: 10.1002/eji.1830201241.

Abstract

Adjuvant arthritis (AA) in rats is an experimentally induced autoimmune disease mediated by T lymphocytes specific for Mycobacterium tuberculosis. We raised the question whether T cells carrying the gamma/delta T cell receptor (TcR), reactive or not to mycobacterial antigens, are involved in the pathogenesis of AA. For this purpose, T cells bearing the TcR alpha/beta were depleted from circulation by treatment with a monoclonal antibody against the rat TcR alpha/beta (R73). This treatment efficiently suppressed existing disease. Even more efficient was pretreatment with R73 from birth, which prevented AA induction completely. In these alpha/beta+ T cell-depleted animals an elevated level of alpha/beta- T cells (about 15% vs. 1% in normal rats) was evident, which was not significantly increased by Mycobacterium tuberculosis injection. We found no positive evidence that gamma/delta + T cells do contribute to AA induction. Moreover, treatment with an anti-TcR alpha/beta monoclonal antibody may be very efficient treatment of T cell-mediated autoimmune diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / administration & dosage
  • Antibodies, Monoclonal / immunology
  • Antigens, Differentiation / analysis
  • Arthritis, Experimental / immunology
  • Arthritis, Experimental / prevention & control
  • CD5 Antigens
  • Immunity, Cellular
  • Immunization, Passive
  • Rats
  • Rats, Inbred Lew
  • Receptors, Antigen, T-Cell / classification
  • Receptors, Antigen, T-Cell / immunology*
  • T-Lymphocyte Subsets / immunology
  • T-Lymphocytes / immunology*

Substances

  • Antibodies, Monoclonal
  • Antigens, Differentiation
  • CD5 Antigens
  • Receptors, Antigen, T-Cell