Expression of glucocorticoid induced TNF receptor family related protein (GITR) on peripheral T cells from normal human donors and patients with non-infectious uveitis

J Autoimmun. 2003 Aug;21(1):83-92. doi: 10.1016/s0896-8411(03)00085-4.

Abstract

The expression of the glucocorticoid induced TNF receptor family related gene (GITR) in subsets of T lymphocytes from human peripheral blood was studied. In normal human peripheral blood mononuclear cells, GITR expression on the resting CD4+ T cells was low but markedly increased after activation. The percentage of GITR+ T cells in the CD4+CD25+ T cell subpopulation (15.1%) was significantly higher than that in the CD4+CD25- T cell subpopulation (5.2%, P<0.01), suggesting a preferential co-expression of GITR with CD25. In a group of patients with non-infectious uveitis, a proposed T helper cell mediated autoimmune ocular disease, the GITR expression on the CD4+ T cells in both the active patients (34.5%) and the inactive patients (19.6%) was significantly higher as compared to that in the normal donors (10.7%; P<0.01 vs. active, P<0.05 vs. inactive). This increased GITR expression in T cells was only seen in the CD4 positive T helper cell subpopulation but not in the CD4 negative T cell subpopulation. GITR expression on the CD4+ T cells decreased when the patients became clinically quiescent. Therefore, GITR is an activation marker for the CD4+ T cells and preferentially co-expressed with CD25 on the CD4+ T cells in human peripheral blood. Its expression correlates with the clinical course of non-infectious uveitis.

Publication types

  • Comparative Study

MeSH terms

  • Autoimmune Diseases / metabolism*
  • Autoimmune Diseases / physiopathology
  • CD3 Complex / metabolism
  • CD4-Positive T-Lymphocytes / metabolism*
  • Glucocorticoid-Induced TNFR-Related Protein
  • Humans
  • RNA, Messenger / metabolism
  • Receptors, Interleukin-2 / biosynthesis
  • Receptors, Interleukin-2 / genetics
  • Receptors, Nerve Growth Factor / biosynthesis
  • Receptors, Nerve Growth Factor / genetics*
  • Receptors, Tumor Necrosis Factor / biosynthesis
  • Receptors, Tumor Necrosis Factor / genetics*
  • T-Lymphocytes, Helper-Inducer / metabolism
  • Up-Regulation
  • Uveitis / metabolism*
  • Uveitis / physiopathology

Substances

  • CD3 Complex
  • Glucocorticoid-Induced TNFR-Related Protein
  • RNA, Messenger
  • Receptors, Interleukin-2
  • Receptors, Nerve Growth Factor
  • Receptors, Tumor Necrosis Factor
  • TNFRSF18 protein, human