GITR+ regulatory T cells in the treatment of autoimmune diseases

LPS-treated bone marrow-derived dendritic cells induce immune tolerance through modulating differentiation of CD4+ regulatory T cell subpopulations mediated by 3G11 and CD127

“…It has been known that phenotype of conventional T regs is CD4 + CD25 + FoxP3 + T cells [11, 28]. Moreover, GITR is also expressed on surface of typical CD4 + T regs [13]. In addition, 3G11 is a marker for specific subsets of CD4 + T regs [14, 15, 20, 29].…”

“…Multiple T reg -associated molecules have been found since 1990s. For instance, glucocorticoid-induced tumor necrosis factor receptor (GITR) is also a molecular marker expressed on T regs [13]. 3G11, a sialylated carbohydrate epitope of the disialoganglioside molecule, is associated with definition of specific T reg subsets [14, 15]; however, regulatory mechanisms of T reg development and differentiation are still obscure.…”

Induction of regulatory T cells: A role for probiotics and prebiotics to suppress autoimmunity

“…However, a recent review article discussing data from mouse and human studies has suggested that GITR is a crucial player in the differentiation of thymic Tregs (tTregs), and expansion of both tTregs and peripheral Tregs (pTregs) [31]. Moreover, the authors have suggested two potential new approaches for treating autoimmune diseases consisting of the in vivo expansion of GITR + Tregs by GITR-triggering drugs and in vitro expansion of autologous or heterologous GITR + Tregs to be infused in the patients [32].…”

DNMT1 cooperates with MBD4 to inhibit the expression of Glucocorticoid‐induced TNFR‐related protein in human T cells

“…The transcription factor FOXP3 binds to the enhancer region of Gitr and further activates Gitr gene transcription [4,5]. Notably, in the condition of autoimmune diseases, the dysfunction or instability of Treg cells is correlated with a decreased expression of GITR and a hyperactivation of Teff cells [6][7][8][9]. Meanwhile, GITR-deficient mice display a lower number of Treg cells [10].…”