Do CD4+ CD25+ immunoregulatory T cells hinder tumor immunotherapy?

J Immunother. May-Jun 2002;25(3):202-6. doi: 10.1097/00002371-200205000-00002.

Abstract

After years of banishment from mainstream immunology, the notion that one subset of T cells can exert regulatory effects on other T lymphocytes is back in fashion. Recent work in knockout and transgenic mice has begun to bring molecular definition to our understanding of immunoregulatory CD4+CD25+ T cells (Treg/Th3/Tr1). The identification of the glucocorticoid-induced tumor necrosis factor receptor family-related gene (GITR, also known as TNFRSF18) expressed on T regulatory cells might afford new therapeutic opportunities. Another possible therapeutic intervention could be the blockade of signaling through the molecular pair of tumor necrosis factor-related activation induced cytokine (TRANCE) and receptor activator of NF-kappaB (RANK). Based on the available evidence from experimental mouse tumor models, however, it seems that simply blocking or even eliminating T regulatory function will not be enough to manage established tumors. The challenge for immunotherapists now is to overcome immunosuppression using the knowledge gained through the understanding of T regulatory cell function.

Publication types

  • Editorial
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Autoimmunity
  • CD4 Antigens / analysis
  • CD4 Antigens / physiology*
  • Immune Tolerance
  • Immunotherapy, Adoptive / methods*
  • Lymphocyte Activation
  • Lymphocyte Depletion*
  • Mice
  • Neoplasms / immunology
  • Neoplasms / therapy*
  • Receptors, Interleukin-2 / analysis
  • Receptors, Interleukin-2 / physiology*
  • T-Lymphocytes / immunology*

Substances

  • CD4 Antigens
  • Receptors, Interleukin-2