anti-TNFRSF25 (TNFRSF25) Antikörper

Human Tumor Necrosis Factor Receptor Superfamily, Member 25 (TNFRSF25) Interaktionspartner

1. Hypermethylation of the proapoptotic genes BCL2 L11 and TNFRSF25 is observed in pleomorphic adenoma of the salivary glands. However, this phenomenon did not impact mRNA transcription.

2. the DR3/TL1A pathway directly enhances human OC formation and resorptive activity, controlling expression and activation of CCL3 and MMP-9.

3. Untreated children with IBD have higher percentage of DR3(+) PBMCs.

4. In addition to apoptosis, DR3 can robustly trigger necroptotic cell death and provide evidence for TL1A-induced, DR3-mediated necrosome assembly. DR3-mediated necroptosis critically depends on receptor-interacting protein 1 (RIP1) and RIP3, the core components of the necroptotic machinery, which activate the pseudo-kinase mixed lineage kinase domain-like, the prototypic downstream effector molecule of necroptosis.

5. Data suggest that human regulatory T-lymphocytes express DR3 and demonstrate DR3/TL1A-mediated activation of signaling via MAP kinases and NFkappaB. (DR3 = death receptor 3; TL1A/TNFSF15 = tumor necrosis factor [ligand] superfamily, member 15)

6. These results raise the possibility for involvement of TL1A/DR3/DR3-mediated mechanisms in epithelial-mesenchymal interactions and the development of inflammation-induced intestinal fibrosis in Crohn's disease.

7. Activation of DR3 is accompanied by inhibition of apoptosis of naive T-lymphocytes in children with acute infectious mononucleosis.

8. Biologics beyond TNF-alpha inhibitors and the effect of targeting the homologues TL1A-DR3 pathway in chronic inflammatory disorders.

9. Higher DR3 levels were associated with early stage chronic lymphocytic leukemia.

10. DR3 is efficiently activated by soluble TL1A trimers.

11. These data identify new roles for DR3 in regulating OB-dependent bone mineral apposition.

12. Human memory IL-18Ralpha and DR3 CD4+ T cells may contribute to antigen-independent innate responses at barrier surfaces.

13. DR3 is expressed by IL-22-producing human group 3 innate lymphoid cells (ILC3s).

14. These results suggested that TL1A could promote Th17 differentiation in rheumatoid arthritis via the activation of RORc, and this effect may be mediated by the binding of TL1A with DR3.

15. Silencing of the DR3 gene affect levels of apoptosis antigen3 ligand in cells.

16. DR3 is expressed in some interstitial vascular endothelial cells in human kidney in situ. These EC also respond to TL1A by activating NF-kappaB. Very low levels of DR3 are seen on the cell surface of HUVEC, which do not respond to TL1A.

17. The changes in frequency of occurrence of spliced variants of DR3/LARD mRNA were directed towards modulation of apoptosis and restraint of antiviral immune response.

18. Distinctions in occurrence of spectrums of DR3/LARD mRNA at healthy volunteers and colon cancer patients can define a different susceptibility of immunocompetent and tumor cells for apoptosis

19. DR-3 drives early cartilage destruction in the antigen-induced model of inflammatory arthritis through the release of CXCL1, maximizing neutrophil recruitment to the joint and leading to enhanced local production of cartilage-destroying enzymes.

20. Suggest tectochrysin leads to apoptotic cell death in NSCLC cells through activation of DR3 and Fas expression via inhibition of STAT3 phosphorylation.

Mouse (Murine) Tumor Necrosis Factor Receptor Superfamily, Member 25 (TNFRSF25) Interaktionspartner

1. in vivo targeting of the TNF superfamily receptor TNFRSF25 using the TL1A-Ig fusion protein, along with IL-2, resulted in transient but massive Treg expansion in donor mice; transplantation of Treg-expanded donor cells facilitated transplant tolerance without GVHD, with complete sparing of graft-versus-malignancy.

2. the DR3/TL1A pathway directly enhances human OC formation and resorptive activity, controlling expression and activation of CCL3 and MMP-9.

3. DR3ko mice were resistant to cellular accumulation within the alveolar passages in acute, but not chronic allergic lung inflammation, and displayed reduced goblet cell hyperplasia in chronic, but not acute allergic lung inflammation

4. This work describes both a novel function and essential requirement for the DR3/TL1A pathway in acute, resolving, and chronic inflammation in the peritoneal cavity.

5. this study shows that DR3 signaling protects mice from acute dextran sodium sulfate colitis because DR3-/- mice showed more severe mucosal inflammation and increased mortality

6. the critical effect of the state of T-cell activation on clinical outcomes after activation of DR3, is reported.

7. These data identify new roles for DR3 in regulating OB-dependent bone mineral apposition.

8. Data indicate that death receptor 3 (DR3) depletion gives rise to an increased anti-apoptotic potential.

9. these data identify TL1A-DR3 interactions as a novel pathway that promotes Th9 differentiation and pathogenicity. TL1A may be a potential therapeutic target in diseases dependent on IL-9.

10. TL1A induces NF-kappaB activation in EC in renal and cardiac tissue from wild type but not DR3 knock-out mice.

11. Both in supernatant and as purified fusion protein, TL1A-Ig binds to TNFRSF25 transfected--but not untransfected--P815 tumor cells as determined by flow cytometry.

12. TNFRSF25 agonists expand Tregs in vivo and delay cardiac allograft rejection.

13. TNFRSF25 agonistic antibody and galectin-9 combination therapy controls herpes simplex virus-induced immunoinflammatory lesions

14. This is the first description of DR3 regulating virus-specific T-cell function in vivo and uncovers a critical role for DR3 in mediating antiviral immunity.

15. DR3 signaling protects against cisplatin nephrotoxicity mediated by tumor necrosis factor.

16. DR3 facilitates clearance of Salmonella typhimurium in vivo.

17. The Ron receptor promotes prostate tumor growth in the TRAMP mouse model.

18. promotes CD8+ T-cell responses and anti-tumor immunity

19. Our findings identify mechanisms by which chronic DR3 signaling could promote pathogenesis in inflammatory bowel disease.

20. TRADD is required for recruitment of receptor interacting protein 1 and TNFR-associated factor 2 to the DR3 signaling complex and for the ubiquitination of receptor interacting protein 1