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TNFRSF18 encodes a member of the TNF-receptor superfamily. Zusätzlich bieten wir Ihnen TNFRSF18 Antikörper (356) und TNFRSF18 Kits (19) und viele weitere Produktgruppen zu diesem Protein an.
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These results suggest that therapeutically targeting GITR represents a unique approach to cancer immunotherapy and suggests that a multimeric fusion protein may provide increased agonistic potential versus an antibody
These findings support further study into combination partners for GITRL (zeige TNFSF18 Proteine)-FP that may augment CD8 (zeige CD8A Proteine) T-cell priming as well as provide hypotheses that can be tested in human clinical trials exploring GITR agonists including GITRL (zeige TNFSF18 Proteine)-FP.
Expression of human GITR was comparable with that of mouse GITR in tumor-infiltrating Tregs despite being drastically lower in other human TILs and in many human peripheral blood populations.
anti-GITR mAb shifts Treg populations to enable immune attack on tumors, with clinical implications for molecular markers to modify emerging treatments.
Continuous GITR stimulation through B cell Gitrl (zeige TNFSF18 Proteine) acts protective in a mouse model of atherosclerosis by regulating the balance between regulatory and effector memory CD4 (zeige CD4 Proteine)(+) T cells.
these results indicate that blockade of GITR signaling can ameliorate arthritis progression mainly by modulating the follicular helper T cell response
GITR appears as a potential target for intervention during infection by the parasite Toxoplasma gondii, even though further studies are still necessary to better characterize the immune response triggered by GITR activation during T. gondii infection
our data suggest a critical role for GITR in Treg cell homeostasis and indicate that Ptpn22 (zeige PTPN22 Proteine) independently affects the differentiation status of Treg cells and their homeostatic behavior
These findings provide further support for the continued development of agonist anti-GITR antibodies as an immunotherapeutic strategy for osteosarcoma. We suggest that our proposed immunotherapy could be developed further to improve osteosarcoma treatment
Th9 cells and iTregs are developmentally linked and GITR can subvert tolerogenic conditions to boost Th9 immunity.
HTLV-1 infection can modify the expression of main functional transcription factors, FOXP3 (zeige FOXP3 Proteine) and GITR
a novel molecular mechanism by which MBD4 (zeige MBD4 Proteine) inhibits GITR expression in a DNMT1 (zeige DNMT1 Proteine)-dependent manner
Aberrant expression of GITR may contribute to systemic lupus erithematosus pathogenesis. Glucocorticoid may achieve its therapeutic effect partly by inducing GITR expression on Tresps rather than Tregs, which initiates the apoptosis of Tresp cells in SLE patients.
GITR expression can enhance the sensitivity to Bortezomib by inhibiting Bortezomib-induced NF-kappaB (zeige NFKB1 Proteine) activation.
GITR is a crucial player in differentiation of thymic regulatory T cells and expansion of regulatory T cells, including both thymic regulatory T cells and peripheral regulatory T cells.
Data may suggest a key role of regulatory GITR+CD25 (zeige IL2RA Proteine) low/-CD4 (zeige CD4 Proteine)+ T cells subset in the modulation of the abnormal immune response in lupus erythematosus (SLE) patients.
results suggest that the GITR rs3753348 polymorphism may be involved in the development and susceptibility of CWP.
these results show a higher susceptibility to apoptosis in patients' versus controls' T(reg (zeige EXTL3 Proteine)) cells, suggesting that GITR is a T(reg (zeige EXTL3 Proteine))-cell marker that would be primarily involved in T(reg (zeige EXTL3 Proteine))-cell survival rather than in their suppressor function.
Our findings indicate the possible involvement of GITR-GITRL (zeige TNFSF18 Proteine) pathway in the pathogenesis of pSS (zeige CDSN Proteine).
GITR acts as a potential tumor suppressor in MM.
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.
tumor necrosis factor receptor superfamily member 18
, glucocorticoid-induced TNFR-related
, tumor necrosis factor receptor superfamily, member 18
, glucocorticoid-induced TNFR-related protein
, TNF receptor superfamily activation-inducible protein
, activation-inducible TNFR family receptor