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Review
. 2020 Oct 9:11:588682.
doi: 10.3389/fimmu.2020.588682. eCollection 2020.

The Role of GITR/GITRL Interaction in Autoimmune Diseases

Jie Tian  1   2 , Beibei Zhang  2 , Ke Rui  3 , Shengjun Wang  1   2
Affiliations
Review

The Role of GITR/GITRL Interaction in Autoimmune Diseases

Jie Tian et al. Front Immunol. .

Abstract

Glucocorticoid-induced TNFR-related protein (GITR) is a member of the TNFR superfamily which is expressed in various cells, including T cells, natural killer cells and some myeloid cells. GITR is activated by its ligand, GITRL, mainly expressed on antigen presenting cells and endothelial cells. It has been acknowledged that the engagement of GITR can modulate both innate and adaptive immune responses. Accumulated evidence suggests GITR/GITRL interaction is involved in the pathogenesis of tumor, inflammation and autoimmune diseases. In this review, we describe the effects of GITR/GITRL activation on effector T cells, regulatory T cells (Tregs) and myeloid cells; summarize its role and the underlying mechanisms in modulating autoimmune diseases.

Keywords: GITRL; T cell; autoimmune diseases; glucocorticoid-induced TNFR-related protein; myeloid cells.

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Figures

Figure 1
Figure 1
Effects of Glucocorticoid-induced TNFR-related protein (GITR) triggering in effector T cells and Treg cells. Different effects are induced in effector T cells and Treg cells after GITR triggering by GITR ligand (GITRL) or agonist anti-GITR Ab (DTA-1). Triggering GITR can promote the differentiation and proliferation of Th17, Th9, and Tfh cells.
Figure 2
Figure 2
Effects of Glucocorticoid-induced TNFR-related protein (GITR)/GITR ligand (GITRL) activation in myeloid cells. Multiple effects of GITR triggering by agonist anti-GITR Ab (DTA-1) or engagement by soluble/membrane GITR in DCs and macrophages. Activation of GITR by GITRL impairs the suppressive function of MDSCs.
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