anti-TNFRSF1B (TNFRSF1B) Antikörper

Human Tumor Necrosis Factor Receptor Superfamily, Member 1B (TNFRSF1B) Interaktionspartner

1. our data provides a novel insight about the complex interplay between Th17 and Treg subsets in which Th17 cells potentially stimulate the increased frequency of Tregs. This effect is mainly mediated by TNF-alpha-TNFR2 signaling pathway.

2. TNFR2 diverts the tumor-inhibiting TNF into a tumor-advocating factor. TNFR2 directly promotes the proliferation of some kinds of tumor cells. Also activating immunosuppressive cells, it supports immune escape and tumor development.

3. Increase in serum sTNFR II level and elevated sTNFR II/I ratio may be promising indicators of the development of coronary artery lesions in Kawasaki disease.

4. Both CD4+ and CD8+ human Treg cells were most efficiently expanded in the presence of TNFRII activation.

5. this paper shows association of TNFRSF1B promoter polymorphisms with autoimmune diseasse

6. From these experiments, we gained no evidence for inhibitory effects of high concentrations (20-500 nM) of PGRN on the interaction of TNF with TNFR1 and TNFR2.

7. Data suggest that an autocrine tumor necrosis factor-alpha (TNFalpha)-tumor necrosis factor receptor 2 (TNFR2) loop plays an important role in endorsing Treg cell stability.

8. It can be concluded that the mRNA levels of TNFR1 and TNFR2 were not associated with coronary artery disease risk

9. In rotenone-mediated dopaminergic cell models, the enhancement of p75 contributed to alpha-syn expression. The elevation of p75 also boosts the expression of ubiquitin ligase absentia homolog (siAH) and nuclear p65. Thus, p75 may enhance alpha-syn expression by promoting the activation of siAH, which is associated with ubiquitination.

10. The soluble TNF-RII/I ratio increased profoundly as macrophage activation syndrome developed and correlated positively with disease activity

11. The aim of current study was to explore longitudinally the prevalence, severity, potential factors, and predictors of depression among Chinese Han adolescent survivors with different genotypes of tumor necrosis factor receptor-II (TNF-RII) rs1061622 after the 2008 Wenchuan earthquake

12. The case-control study (401 patients and 657 controls) revealed that the genetic variants of rs3397, rs1061622, and rs1061624 in the TNFR2 gene are associated with a higher risk of developing schizophrenia and more severe course in men.

13. Elevated TNFRs levels were associated with the risk of cardiovascular and/or all-cause mortality independent of all relevant covariates in patients undergoing haemodialysis

14. TL1A modulated Rheumatoid arthritis-fibroblast-like synoviocytes migration and Indian hedgehog signaling pathway using TNFR2.

15. Genotype rs767455 was associated with the susceptibility of ankylosing spondylitis(AS), G allele of rs767455 exhibited an association with the risk of developing AS. Only rs1061622 was significantly associated with long-term efficacy of etanercept. The results suggest that TNFRSF1A and TNFRSF1B polymorphisms were associated with susceptibility, severity, and the long-term therapeutic efficacy of etanercept of AS patients.

16. Data suggest that maternal glycemic response during pregnancy is associated with lower DNA methylation of 4 CpG sites within PDE4B gene in placenta (collected after normal-weight term birth); 3 additional CpG sites are differentially methylated relative to maternal glucose response within TNFRSF1B, LDLR, and BLM genes. (PDE4B = phosphodiesterase-4B; LDLR = low density lipoprotein receptor; BLM = Bloom syndrome protein)

17. serum level did not change after tonsillectomy alone but decreased significantly after steroid pulse therapy in patients with IgA nephropathy

18. Elevated serum TNFR2 may be a possible marker of COPD in asymptomatic smokers and ex-smokers.

19. TNFR2 promoted Adriamycin resistance in breast cancer cells by regulating the DNA damage repair.

20. Serum TNFR2 is a biomarker for patients with chronic kidney disease.

Cow (Bovine) Tumor Necrosis Factor Receptor Superfamily, Member 1B (TNFRSF1B) Interaktionspartner

1. These results show an unclear effect of considered T>C polymorphism on TNF-RII gene expression in bovine leukocytes and they suggest the involvement of BLV in modifying the TNF-RII expression in BLV-infected cows.

2. These results suggest that the endometrium might lower the TNF concentration in the blastocyst by (1) regulating TNF secretion into the uterine fluid and (2) inducing decreased TNF and TNFR2 mRNA transcription in the embryo.

3. These results suggest that TNF-alpha sources include immune cells, as well as large and small luteal cells, and that TNF-RI and TNF-RII are present in the luteal cells of the bovine corpus luteum.

4. The expression and cellular localization of tumor necrosis factor-alpha (TNF) and its receptors (TNFRI and TNFRII) mRNAs and proteins, were determined.[TNFRII]

Pig (Porcine) Tumor Necrosis Factor Receptor Superfamily, Member 1B (TNFRSF1B) Interaktionspartner

1. Retinal ischemia results in increased expression of TNF-alpha and its receptors (TNF-R1 and TNF-R2).

2. Porcine TNFR2 (1,125 bp, 375 amino acid residues), which contains specific amino acid region of transmembrane, indicated high identities with human and murine TNFR2

3. pTNFR2 isoforms may play differential roles in the process of xenograft rejection.

Mouse (Murine) Tumor Necrosis Factor Receptor Superfamily, Member 1B (TNFRSF1B) Interaktionspartner

1. Selective activation of TNFRII was found to expand both CD4+ and CD8+ Treg cells. TNFRII activation elevated the number of CD4+CD25+ and CD8+CD25+ Treg cells and increased the number of FoxP3-expressing cells in CD8+, but not CD4+, Treg cells. In the experimental arthritis model, TNFRII activation led to the expansion of both CD4+ and CD8+ Treg cells in vivo and induced antiinflammatory responses that alleviated arthritis

2. Toll like receptor-4 (TLR4) and tumor necrosis factor receptor type II (TNFR2)-dependent mechanisms, but not IL-10-dependent pathways, modulate the anti-inflammatory response of CD4+ Tregs following trauma.

3. In conclusion, these data provide evidence for a regulatory role of TNF-alpha in diesel exhaust particles-induced pulmonary inflammation and identify TNFR2 as the most important receptor in mediating these inflammatory effects.

4. Atherosclerotic pathology in each Chlamydia pneumoniae (CPN)-infected knockout (KO)mouse group was reduced significantly compared to WT mice, suggesting that both TNFR1 and TNFR2 promote CPN-induced atherosclerosis.

5. MPTP induced TNF-alpha signaling through TNFR2 mediated pathway and recruited p65-p52 dimer in hippocampal nucleus which is reported to have protective effect on hippocampal neurons indicated by unchanged neuronal count in hippocampus in treated groups with respect to control.

6. Recognition memory improved with exercise in WT mice, was impaired in TNFR1(-/-) exercise mice, showed non-significant impairment with exercise in TNF(-/-) mice, and no changes in TNFR2(-/-) mice. In spatial learning there were exercise related improvements in WT mice, non-significant but meaningful impairments evident in TNFR1(-/-) exercise mice, modest improvement in TNF(-/-) exercise mice.

7. TNFR2 sensitizes macrophages for endogenous TNF-induced TNFR1-mediated necroptosis

8. study reports an important role for TNFR2 on low-affinity-primed secondary effector CD8+ T cells; results demonstrate the importance of TNF signaling in low-affinity, cross-reactive CD8+ T cell responses during heterologous immunity

9. TNF plays an inhibitory role in modulating myocardial SDF-1 production and blockade of TNF signaling by ablation of TNFR1 and TNFR2 genes increased SDF-1 expression in the heart. These data expand on TNF signaling-initiated mechanisms in myocardium, which may lend a more complete understanding of SDF-1 and TNFR-derived actions in hopes of advancing ischemic heart injury treatments.

10. Results suggest that elevated TNF in the heart, via TNFR1 and TNFR2, restrains cardiomyocyte differentiation of resident cardiac stem cells and may enhance adrenergic activation, both effects that would reduce the effectiveness of endogenous cardiac repair and the response to exogenous stem cell therapy, while promoting adverse cardiac remodeling.

11. Report chronic inflammatory multiorgan hepatobiliary pancreatitis, along with fibrosis and calculi formation induced by oral dibutyltin administration in TNFR1/R2 deficient mice.

12. These findings implicate TNF-receptor signaling cascades in the regulation of homeostatic plasticity of denervated networks and suggest an important role for TNFalpha-signaling in the course of neurological diseases accompanied by deafferentation.

13. TNF receptor 1 (TnfR1) signaling is believed to be a major mediator of the cytotoxicity of Tnf-a through activation of caspases.

14. our findings implicate TNFR2 in supporting myeloid-derived suppressor cells -mediated immune suppression and metastasis in the liver

15. TNFR2 blockade appears to disrupt commensal bacteria-host immune symbiosis to reveal autoimmune demyelination in genetically susceptible mice.

16. TNFR2 protects mice from colitis by inhibiting the expansion of colonic CD8(+) T cells.

17. Collectively, these results demonstrate that TNFR2-bearing CD8(+) T cells and TNFR1-bearing non-CD8(+) T cells contribute significantly to oviduct pathology following genital chlamydial infection.

18. To determine the role of TNF-TNFR2/p75 signaling in ischemia-induced inflammation and muscle regeneration, we subjected wild-type and TNFR2/p75 knockouts to hind limb ischemia.

19. Results demonstrate novel roles of TNFRII in the regulation of Abeta production, suggesting a potential therapeutic strategy for Alzheimer's disease by up-regulating TNFRII levels and elevating phosphorylated IkappaBalpha by SUMOylation.

20. PGRN protection of endoplasmic reticulum stress induced apoptosis was abolished when TNFR2 signaling was blocked.

Zebrafish Tumor Necrosis Factor Receptor Superfamily, Member 1B (TNFRSF1B) Interaktionspartner

1. Targeted gene knockdown of TNFRSF1B in zebrafish embryos results in the induction of a caspase-8, caspase-2 and P53-dependent apoptotic program in endothelial cells that bypasses caspase-3.