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Engagement of glucocorticoid-induced TNFR family-related receptor on effector T cells by its ligand mediates resistance to suppression by CD4+CD25+ T cells

J Immunol. 2004 Oct 15;173(8):5008-20. doi: 10.4049/jimmunol.173.8.5008.

Abstract

Nonactivated CD4+CD25+ regulatory T cells constitutively express glucocorticoid-induced TNFR family-related receptor (GITR), a TNFR family member whose engagement was presumed to abrogate regulatory T cell-mediated suppression. Using GITR-/- mice, we report that GITR engagement on CD25-, not CD25+ T cells abrogates T cell-mediated suppression. Mouse APCs constitutively express GITR ligand (GITR-L), which is down-regulated following TLR signaling in vivo. Although GITR-/-CD25- T cells were capable of mounting proliferative responses, they were incapable of proliferation in the presence of physiological numbers of CD25+ T cells. Thus, GITR-L provides an important signal for CD25- T cells, rendering them resistant to CD25+ -mediated regulation at the initiation of the immune response. The down-regulation of GITR-L by inflammatory stimuli may enhance the susceptibility of effector T cells to suppressor activity during the course of an infectious insult.

MeSH terms

  • Animals
  • CD28 Antigens / physiology
  • CD4 Antigens / analysis*
  • Carrier Proteins / physiology*
  • Glucocorticoid-Induced TNFR-Related Protein
  • Humans
  • Ligands
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Receptors, Interleukin-2 / analysis*
  • Receptors, Nerve Growth Factor / physiology*
  • Receptors, Tumor Necrosis Factor / physiology*
  • T-Lymphocytes, Regulatory / physiology*
  • Tumor Necrosis Factors

Substances

  • CD28 Antigens
  • CD4 Antigens
  • Carrier Proteins
  • Glucocorticoid-Induced TNFR-Related Protein
  • Ligands
  • Receptors, Interleukin-2
  • Receptors, Nerve Growth Factor
  • Receptors, Tumor Necrosis Factor
  • TNFRSF18 protein, human
  • Tnfrsf18 protein, mouse
  • Tnfsf18 protein, mouse
  • Tumor Necrosis Factors