Disease relevance of Tnfsf18

• This report evaluates the role of interaction between glucocorticoid-induced tumor necrosis factor receptor (GITR) and GITR ligand (GITR-L) in the immuno-inflammatory response to infection with herpes simplex virus (HSV) [1].
• B cells suppressed autoimmunity by maintenance of regulatory T cells via GITRL [2]

High impact information on Tnfsf18

• RT-PCR and mAb staining revealed mouse GITR ligand expression in dendritic cells, macrophages, and B cells [3].
• GITR-mediated stimulation induced by anti-GITR mAb DTA-1 or GITR ligand transfectants efficiently augmented the proliferation of both CD25-CD4+ and CD25+CD4+ T cells under the limited dose of anti-CD3 stimulation [4].
• In vivo kinetics of GITR and GITR ligand expression and their functional significance in regulating viral immunopathology [1].
• GITR and GITR ligand were expressed constitutively on the surface of Raw 264.7 macrophage cell line and murine peritoneal macrophages [5].
• We have inserted the sequences for natural, membrane-bound GITR-ligand (GITR-L) and a truncated secreted form of GITR-L (GITR-Lsol) into the adenovirus-5 genome [6].
• B cells suppressed autoimmunity by maintenance of regulatory T cells via GITRL [2]  

Anatomical context of Tnfsf18

• GITR ligand (GITRL) is expressed in several cells including macrophages, B cells, dendritic cells, and endothelial cells [7].
• GITR ligand and GITR were expressed constitutively on the surface of spleen cells and cells from peritoneal fluid [8].

Associations of Tnfsf18 with chemical compounds

• Macaque Multimeric Soluble CD40 Ligand and GITR Ligand Constructs Are Immunostimulatory Molecules In Vitro [9].
• Modulation of tryptophan catabolism via the GITR-GITRL coreceptor system might represent an effective therapeutic target in immune regulation [10].

References