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The protein encoded by TNFSF18 is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. Zusätzlich bieten wir Ihnen Tumor Necrosis Factor (Ligand) Superfamily, Member 18 Antikörper (184) und Tumor Necrosis Factor (Ligand) Superfamily, Member 18 Kits (14) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 38 products:
Human TNFSF18 Protein expressed in HEK-293 - ABIN2666573
Azuma: Role of the glucocorticoid-induced TNFR-related protein (GITR)-GITR ligand pathway in innate and adaptive immunity. in Critical reviews in immunology 2010
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Human TNFSF18 Protein expressed in Escherichia coli (E. coli) - ABIN667587
Gurney, Marsters, Huang, Pitti, Mark, Baldwin, Gray, Dowd, Brush, Heldens, Schow, Goddard, Wood, Baker, Godowski, Ashkenazi: Identification of a new member of the tumor necrosis factor family and its receptor, a human ortholog of mouse GITR. in Current biology : CB 1999
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GITRL levels are significantly elevated in rheumatoid arthritis serum and synovial fluid and are positively correlated with autoantibody production in rheumatoid arthritis, suggesting a role of GITRL in the development of rheumatoid arthritis.
GITRL modulates the activities of p38 MAPK (zeige MAPK14 Proteine) and STAT3 (zeige STAT3 Proteine) to promote Th17 cell differentiation in autoimmune arthritis.
An increase in GITRL may impair the balance of Th17/Treg, and contribute to the pathopoiesis of Hashimoto's thyroiditis.
Our findings indicate the possible involvement of GITR (zeige TNFRSF18 Proteine)-GITRL pathway in the pathogenesis of pSS (zeige CDSN Proteine).
Serum GITRL levels were higher in SLE patients.
Glucocorticoid-induced TNF-related ligand (GITRL) confers pseudoexpression to tumor cells by platelets, which results in GITRL expression by megakaryocytes and their platelet progeny.
observation suggests a link between cytokine-regulated keratinocyte GITRL expression and its role in inflammatory responses in AD
GITRL upregulation induced by IFN-beta (zeige IFNB1 Proteine) on dendritic cells downregulates CTLA-4 (zeige CTLA4 Proteine) on regulatory T (Treg) cells, facilitating proliferation of anergic Treg cells in multiple sclerosis treatment of multiple sclerosis patients.
Although GITR (zeige TNFRSF18 Proteine) transgene costimulation can therapeutically enhance T helper (Th) type 2 cell responses, GITR-GITR (zeige TNFRSF18 Proteine) ligand interactions are not required for development of Th2-mediated resistance or pathology.
GITRL expression on Kupffer cells may mediate acute rejection in liver transplantation
the upregulation of IFN-beta (zeige IFNB1 Proteine) in DCs induces the up-regulation of coinhibitory molecules B7H1 (zeige CD274 Proteine) and GITRL, which cause an impaired activation of naive Ag-specific T cells
GITRL expressed on macrophages drives cytokine release and T cell activation, resulting in neuropathic pain via GITR (zeige TNFRSF18 Proteine)-dependent actions. The GITRL-GITR (zeige TNFRSF18 Proteine) pathway might represent a novel target for the treatment of neuropathic pain.
Down-regulation of GITRL enhances CD8 (zeige CD8A Proteine) T cell responses to chronic lymphocytic choriomeningitis virus.
Sjogren's syndrome-like autoimmune sialadenitis in MRL-Faslpr mice is associated with expression of glucocorticoid-induced TNF receptor-related protein (GITR) ligand and 4-1BB ligand (zeige TNFSF9 Proteine).
GITRL triggering in endothelial cells increases leukocyte adhesion and transmigration.
The B7H1 (zeige CD274 Proteine) and GITRL molecules may play an important role in TGF-beta (zeige TGFB1 Proteine)-induced Treg expansion of lung cancer microenvironment.
results demonstrate that enhanced GITR (zeige TNFRSF18 Proteine)/GITRL interactions have a pleiotropic role on the regulation of T-cell responses
B cell expression of GITRL induced Treg proliferation, maintaining their numbers above a threshold required for the prevention of autoimmunity.
Findings suggest GITRL could enhance the immune stimulation of DC and might facilitate the potential development of DCs-based anti-tumor therapies.
GITRL-dependent expansion of Treg within the cornea is one mechanism underlying immune privilege in corneal allografts.
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This cytokine is a ligand for receptor TNFRSF18/AITR/GITR. It has been shown to modulate T lymphocyte survival in peripheral tissues. This cytokine is also found to be expressed in endothelial cells, and is thought to be important for interaction between T lymphocytes and endothelial cells.
, GITR ligand
, activation-inducible TNF-related ligand
, glucocorticoid-induced TNF-related ligand
, glucocorticoid-induced TNFR-related protein ligand
, tumor necrosis factor ligand superfamily member 18
, glucocorticoid-induced-tumor necrosis factor receptor ligand