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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 Proteine (37) und Tumor Necrosis Factor (Ligand) Superfamily, Member 18 Kits (16) und viele weitere Produktgruppen zu diesem Protein an.
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Human Monoclonal TNFSF18 Primary Antibody für FACS - ABIN4897643
Han, ONeil-Andersen, Zurier, Lawrence: CD4+CD25high T cell numbers are enriched in the peripheral blood of patients with rheumatoid arthritis. in Cellular immunology 2008
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Mouse (Murine) Monoclonal TNFSF18 Primary Antibody für FACS, ELISA - ABIN2473796
Matsumoto, Ueshima, Ohuchi, Takeuchi, Okabe: Induction of gastric lesions by 2-deoxy-D-glucose in rats following chemical ablation of capsaicin-sensitive sensory neurons. in Japanese journal of pharmacology 1993
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Mouse (Murine) Monoclonal TNFSF18 Primary Antibody für FACS - ABIN2689521
Igarashi, Cao, Iwai, Piao, Kamimura, Hashiguchi, Amagasa, Azuma: GITR ligand-costimulation activates effector and regulatory functions of CD4+ T cells. in Biochemical and biophysical research communications 2008
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Mouse (Murine) Monoclonal TNFSF18 Primary Antibody für FACS - ABIN2473798
Cobbold, Castejon, Adams, Zelenika, Graca, Humm, Waldmann: Induction of foxP3+ regulatory T cells in the periphery of T cell receptor transgenic mice tolerized to transplants. in Journal of immunology (Baltimore, Md. : 1950) 2004
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Human Monoclonal TNFSF18 Primary Antibody für FACS - ABIN4897645
Wang, Yi, Qin, Maldonado, von Andrian, Kulkarni, Tellides, Pober: Rapamycin-treated human endothelial cells preferentially activate allogeneic regulatory T cells. in The Journal of clinical investigation 2013
the upregulation of IFN-beta (zeige IFNB1 Antikörper) in DCs induces the up-regulation of coinhibitory molecules B7H1 (zeige CD274 Antikörper) 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 Antikörper)-dependent actions. The GITRL-GITR (zeige TNFRSF18 Antikörper) pathway might represent a novel target for the treatment of neuropathic pain.
Down-regulation of GITRL enhances CD8 (zeige CD8A Antikörper) 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 Antikörper).
GITRL triggering in endothelial cells increases leukocyte adhesion and transmigration.
The B7H1 (zeige CD274 Antikörper) and GITRL molecules may play an important role in TGF-beta (zeige TGFB1 Antikörper)-induced Treg expansion of lung cancer microenvironment.
results demonstrate that enhanced GITR (zeige TNFRSF18 Antikörper)/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.
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 Antikörper) and STAT3 (zeige STAT3 Antikörper) 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 Antikörper)-GITRL pathway in the pathogenesis of pSS (zeige CDSN Antikörper).
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 Antikörper) on dendritic cells downregulates CTLA-4 (zeige CTLA4 Antikörper) on regulatory T (Treg) cells, facilitating proliferation of anergic Treg cells in multiple sclerosis treatment of multiple sclerosis patients.
Although GITR (zeige TNFRSF18 Antikörper) transgene costimulation can therapeutically enhance T helper (Th) type 2 cell responses, GITR-GITR (zeige TNFRSF18 Antikörper) 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 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.
, glucocorticoid-induced TNF-related ligand
, glucocorticoid-induced-tumor necrosis factor receptor ligand
, tumor necrosis factor ligand superfamily member 18
, AITR ligand
, activation-inducible TNF-related ligand
, glucocorticoid-induced TNFR-related protein ligand
, tumor necrosis factor (ligand) superfamily, member 18
, tumor necrosis factor ligand 2A
, tumor necrosis factor superfamily member 18