Regulation of autoimmune response

Curr Opin Immunol. 1994 Dec;6(6):946-55. doi: 10.1016/0952-7915(94)90018-3.

Abstract

Recent work on such apparently disparate fields as T-cell receptor peptide-induced regulation, superantigens, antigen-induced tolerance, models of peripheral tolerance, apoptosis, and T-cell receptor antagonists demonstrates a similarity in immune response from a regulatory perspective. In many systems, a 'tolerance' pathway is observed, characterized broadly as an initial disturbance in the immune system, with a resulting predominance of effector cells, followed by a homeostatic response (often requiring CD8+ cells) which leads the effector population into T-cell receptor downregulation, T-cell inactivation, anergy and, often, eventual apoptotic death. In the regulated immune response, mixed populations of anergized and apoptosing T cells can be found. In some cases, anergy appears to lead to death while, in other instances, cells revert to a functional state. This review focuses on recent papers examining each of these topics in an attempt to obtain a preliminary integrated picture of immune regulation in autoimmune diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Autoantigens / immunology
  • Autoimmune Diseases / immunology*
  • Autoimmunity
  • Cytokines
  • Humans
  • Immune Tolerance
  • Major Histocompatibility Complex / immunology
  • Receptors, Antigen, T-Cell / immunology
  • Superantigens / immunology

Substances

  • Autoantigens
  • Cytokines
  • Receptors, Antigen, T-Cell
  • Superantigens