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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Tumor necrosis factor receptor superfamily, member 18

This gene encodes a member of the TNF-receptor superfamily. The encoded receptor has been shown to have increased expression upon T-cell activation, and it is thought to play a key role in dominant immunological self-tolerance maintained by CD25(+)CD4(+) regulatory T cells. Knockout studies in mice also suggest the role of this receptor is in the regulation of CD3-driven T-cell activation and programmed cell death. Three alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported. [provided by RefSeq, Feb 2011] (from NCBI)
Top mentioned proteins: Foxp3, CD25, CD4, CTLA-4, CAN
Papers on GITR
Trypanosoma cruzi Experimental Infection Impacts on the Thymic Regulatory T Cell Compartment.
Pérez et al., Rosario, Argentina. In Plos Negl Trop Dis, Jan 2016
Moreover, tTregs enhance after the infection the expression of signature markers (CD25, CD62L and GITR) and they also display alterations in the expression of migration-associated molecules (α chains of VLAs and chemokine receptors) such as functional fibronectin-driven migratory disturbance.
Decidual vascular endothelial cells promote maternal-fetal immune tolerance by inducing regulatory T cells through canonical Notch1 signaling.
Liu et al., Wuhan, China. In Immunol Cell Biol, Jan 2016
Consistent with the promotion of Treg cell maintenance and differentiation, Treg cell-associated gene expression such as TGF-β, Ebi3, CD39 and GITR was also increased in the presence of DVECs.
Xenograft of Human Umbilical Mesenchymal Stem Cells from Wharton's Jelly as a Potential Therapy for Rat Pilocarpine-Induced Epilepsy.
Lin et al., Taipei, Taiwan. In Brain Behav Immun, Jan 2016
Implanted HUMSCs survived in the hippocampus and released cytokines, including FGF-6, amphiregulin, glucocorticoid-induced tumor necrosis factors receptor (GITR), MIP-3β, and osteoprotegerin.
The Role of Anti-drug Antibodies in the Pharmacokinetics, Disposition, Target Engagement, and Efficacy of a GITR Agonist Monoclonal Antibody in Mice.
Escandon et al., In J Pharmacol Exp Ther, Jan 2016
DTA-1, an agonist monoclonal antibody against the glucocorticoid-induced TNF receptor-related protein (GITR) is a highly effective antitumor treatment in preclinical models.
GITRL modulates the activities of p38 MAPK and STAT3 to promote Th17 cell differentiation in autoimmune arthritis.
Wang et al., Zhenjiang, China. In Oncotarget, Jan 2016
UNASSIGNED: The glucocorticoid-induced TNFR family-related protein (GITR) and its ligand play a critical role in the pathogenesis of autoimmune arthritis by enhancing the Th17 cell response, but their molecular mechanisms remain largely unclear.
Glucocorticoid-induced tumor necrosis factor receptor-related protein co-stimulation facilitates tumor regression by inducing IL-9-producing helper T cells.
Kang et al., Seoul, South Korea. In Nat Med, Sep 2015
T cell stimulation via glucocorticoid-induced tumor necrosis factor receptor (TNFR)-related protein (GITR) elicits antitumor activity in various tumor models; however, the underlying mechanism of action remains unclear.
Agonists of Co-stimulation in Cancer Immunotherapy Directed Against CD137, OX40, GITR, CD27, CD28, and ICOS.
Melero et al., Pamplona, Spain. In Semin Oncol, Aug 2015
Co-stimulatory receptors include surface moieties that are constitutively expressed on resting lymphocytes such as CD28 or CD27 and others whose expression is induced upon recent previous antigen priming, ie, CD137, GITR, OX40, and ICOS.
GITR+ regulatory T cells in the treatment of autoimmune diseases.
Riccardi et al., Perugia, Italy. In Autoimmun Rev, Feb 2015
In this review, we present data from murine and human studies suggesting that 1) glucocorticoid-induced tumor necrosis factor receptor-related protein (GITR) plays a crucial role in thymic Treg (tTreg) differentiation and expansion; 2) GITR plays a crucial role in peripheral Treg (pTreg) expansion; 3) in patients with Sjögren syndrome and systemic lupus erythematosus, CD4(+)GITR(+) pTregs are expanded in patients with milder forms of the disease; and 4) GITR is superior to other cell surface markers to differentiate Tregs from other CD4(+) T cells.
Glucocorticoid-induced tumour necrosis factor receptor-related protein: a key marker of functional regulatory T cells.
Riccardi et al., Perugia, Italy. In J Immunol Res, 2014
Glucocorticoid-induced tumour necrosis factor receptor-related protein (GITR, TNFRSF18, and CD357) is expressed at high levels in activated T cells and regulatory T cells (Tregs).
Impact of tumour microenvironment and Fc receptors on the activity of immunomodulatory antibodies.
Quezada et al., London, United Kingdom. In Trends Immunol, 2014
This mechanism appears to be common to other immunomodulatory antibodies including those targeting OX40 and glucocorticoid-induced TNFR-related protein (GITR).
Costimulation via the tumor-necrosis factor receptor superfamily couples TCR signal strength to the thymic differentiation of regulatory T cells.
Farrar et al., Minneapolis, United States. In Nat Immunol, 2014
We found here that Treg cell progenitors had high expression of the TNFRSF members GITR, OX40 and TNFR2.
The importance of animal models in tumor immunity and immunotherapy.
Merghoub et al., New York City, United States. In Curr Opin Genet Dev, 2014
co-stimulation such as anti-GITR and anti-OX40).
IκB(NS) protein mediates regulatory T cell development via induction of the Foxp3 transcription factor.
Schmitz et al., Braunschweig, Germany. In Immunity, 2013
Importantly, IκB(NS) was required for the transition of immature GITR(+)CD25(+)Foxp3(-) thymic Treg cell precursors into Foxp3(+) cells.
IL-15-dependent upregulation of GITR on CD8 memory phenotype T cells in the bone marrow relative to spleen and lymph node suggests the bone marrow as a site of superior bioavailability of IL-15.
Watts et al., Toronto, Canada. In J Immunol, 2012
these data suggest that GITR plays a role in the survival of CD8 memory phenotype T cells
Enhanced GITR/GITRL interactions augment IL-27 expression and induce IL-10-producing Tr-1 like cells.
Medley et al., Cambridge, United States. In Eur J Immunol, 2012
results demonstrate that enhanced GITR/GITRL interactions have a pleiotropic role on the regulation of T-cell responses
Loss of T regulatory cell suppression following signaling through glucocorticoid-induced tumor necrosis receptor (GITR) is dependent on c-Jun N-terminal kinase activation.
Gelfand et al., Denver, United States. In J Biol Chem, 2012
Treatment with an inhibitor of JNK phosphorylation resulted in complete reversal of all GITR-induced changes in nTreg phenotype and function, with full restoration of suppression of in vivo lung allergic responses
Glucocorticoid-induced tumor necrosis factor receptor family-related protein regulates CD4(+)T cell-mediated colitis in mice.
Terhorst et al., Boston, United States. In Gastroenterology, 2012
GITR is not required on the surface of CD4-positive T-cells to induce colitis in mice. Knockout mice develop aggravated chronic enterocolitis via an imbalance of colitogenic Th1 cells and Treg cells.
Murine B cell development and antibody responses to model antigens are not impaired in the absence of the TNF receptor GITR.
Pelanda et al., Denver, United States. In Plos One, 2011
Data indicate that GITR does not play a significant role in B cell development and antibody responses to T-dependent and independent model antigens within the context of a GITR-deficient genetic background.
Reverse signaling through GITR ligand enables dexamethasone to activate IDO in allergy.
Puccetti et al., Perugia, Italy. In Nat Med, 2007
Glucocorticoid-induced tumor necrosis factor receptor (GITR) on T cells and its natural ligand, GITRL, on accessory cells contribute to the control of immune homeostasis.
The GITR-GITRL interaction: co-stimulation or contrasuppression of regulatory activity?
Stephens et al., Bethesda, United States. In Nat Rev Immunol, 2006
Stimulation of T cells through GITR (glucocorticoid-induced tumour-necrosis-factor-receptor-related protein) has been shown to enhance immunity to tumours and viral pathogens, and to exacerbate autoimmune disease.
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