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anti-Human TNFSF15 Antibodies:
anti-Mouse (Murine) TNFSF15 Antibodies:
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Human Polyclonal TNFSF15 Primary Antibody for WB - ABIN2476844
Tinkanen, Kujansuu: Doppler ultrasound studies in pelvic inflammatory disease. in Gynecologic and obstetric investigation 1993
Show all 3 Pubmed References
Human Polyclonal TNFSF15 Primary Antibody for IF (p), IHC (p) - ABIN709556
?lebioda, Bojarska-Junak, Stanis?awowski, Cyman, Wierzbicki, Roli?ski, Celi?ski, Kmie?: TL1A as a potential local inducer of IL17A Expression in colon mucosa of inflammatory bowel disease patients. in Scandinavian journal of immunology 2015
significantly higher levels of TL1A and its decoy receptor DcR3 in RA patients than in controls; TL1A is significantly related to the disease activity and enhances IL-17 production
High TL1A expression is associated with coronary artery disease.
Study show that the inflammatory bowel disease (IBD)-risk haplotype at TNFSF15 is associated with decreased expression of the gene by peripheral blood monocytes in both healthy volunteers and IBD patients and suggests that genetically elevated TNFSF15 from monocytes or monocyte-derived cells may protect healthy individuals from the development of IBD.
Discontinuous epitope regions span a distance within the approximate size of the variable domains of mAb1's heavy and light chains, indicating it uses a unique mechanism of action to block the TL1A/DR3 interaction.
TNFSF15 polymorphisms may contribute to genetic susceptibility of inflammatory bowel disease (Meta-Analysis)
TL1A modulated Rheumatoid arthritis-fibroblast-like synoviocytes migration and Indian hedgehog signaling pathway using TNFR2.
TL1A can induce tumor cell proliferation and promote the occurrence of colitis-associated colorectal cancer by activating Wnt/beta-catenin pathway.
TNFSF15, a cytokine mainly produced by blood endothelial cells, facilitates tumor lymphangiogenesis by upregulating VEGFC expression in A549 cells.
Results suggested that TNFSF15 (rs3810936 and rs4979462) SNPs may confer susceptibility to systemic lupus erythematosus (SLE) risk, which were significantly associated with the clinical phenotypes of SLE.
Three alternatively spliced isoforms of VEGI, VEGI174, VEGI192 and VEGI251 have been documented. This study investigated the effects of VEGI174 and its functional domains (V7 and V8) on epithelialmesenchymal transition (EMT) in renal cell carcinoma (RCC) cells in vitro. Overexpression of VEGI174, V7 or V8 inhibited EMT.
Results provide evidence that variance within TNFSF15 has the potential to affect cytokine expression across a range of tissues and thereby contribute to protection from infectious diseases such as leprosy, while increasing the risk of immune-mediated diseases including Crohn's disease and primary biliary cholangitis.
single variant analysis detected a previously unreported psoriasis risk locus at TNFSF15 (rs6478108)
play a role in the development of systemic sclerosis
the DR3/TL1A pathway directly enhances human OC formation and resorptive activity, controlling expression and activation of CCL3 and MMP-9.
the blocking of tumor necrosis factor receptor 2 (TNFR2) decreased TL1A-stimulated IL-6 production by rheumatoid arthritis fibroblast-like synoviocytes.
Distinct but overlapping TNFSF15 haplotypes were demonstrated in diverticulitis patients versus healthy controls when compared with the known Crohn's risk haplotype suggesting similar but distinct genetic predispositions. This study strengthens the role for a genetic predisposition to diverticulitis that involves the TNFSF15 gene.
TL1A differentially induces expression of TH17 effector cytokines IL-17, -9, and -22 and provides a potential target for therapeutic intervention in TH17-driven chronic inflammatory diseases.
Our findings indicate that VEGI174 prevents progression and tumor metastasis through inhibiting epithelial-mesenchymal transition (EMT) in renal cell carcinoma (RCC) in vivo. This may provide a new approach for the treatment of RCC
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)
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.
Tl1a-mediated intestinal fibrosis and fibroblast activation are dependent on specific microbial populations.
These results indicated that constitutive TL1A expression in myeloid cells exacerbated liver fibrosis, probably through macrophage recruitment and secretion of proinflammatory and profibrotic cytokines.
Results indicate a role for group 3 innate lymphoid cell (ILC3) in activating intestinal T cells and a central role for TNF-like ligand 1A (TL1A) in promoting ILC3 barrier immunity during colitis.
These data suggest differential roles for membrane and soluble TL1A on adaptive and innate immune cells
TL1A blocking ameliorates intestinal fibrosis in the T cell transfer model of chronic colitis
ATF3 protects against LPS-induced acute lung injury by inhibiting TL1A expression.
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.
this study shows that TL1A-/- mice are more susceptible to dextran sodium sulfate colitis
These data demonstrated a direct role for TL1A-DR3 signaling in tissue fibrosis and that modulation of TL1A-DR3 signaling could inhibit gut fibrosis.
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.
TL1A induces NF-kappaB activation in EC in renal and cardiac tissue from wild type but not DR3 knock-out mice.
TL1A deficiency impacts on the gut microbial composition and the mucosal immune system, especially the intraepithelial TCRgammadelta(+) T-cell subset, and that TL1A is involved in the establishment of adipose tissue.
Our data demonstrate a key role for TL1A in promoting ILC2s at mucosal barriers.
delivers survival signals to plasma cells and promotes pathogenic Ab production in collagen arthritis
TNFSF15 inhibits vasculogenesis by regulating relative levels of membrane-bound and soluble isoforms of VEGF receptor 1.
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.
These results establish a novel link between tumor necrosis factor (TNF)-family cytokine TL1A (TNFSF15) and interleukin 13 (IL-13) responses that results in small intestinal inflammation.
role of TL1A in mucosal T cells and antigen presenting cells function and showed that up-regulation of TL1A expression can promote mucosal inflammation and gut fibrosis.
findings suggest that the transcription factor NF-kappaB plays an important role in the regulation of VEGI expression
induction of intestinal inflammation is associated with significant up-regulation of TL1A and tm DR3 in the inflamed mucosa
The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. This protein is abundantly expressed in endothelial cells, but is not expressed in either B or T cells. The expression of this protein is inducible by TNF and IL-1 alpha. This cytokine is a ligand for receptor TNFRSF25 and decoy receptor TNFRSF21/DR6. It can activate NF-kappaB and MAP kinases, and acts as an autocrine factor to induce apoptosis in endothelial cells. This cytokine is also found to inhibit endothelial cell proliferation, and thus may function as an angiogenesis inhibitor. Two transcript variants encoding different isoforms have been found for this gene.
tumor necrosis factor ligand superfamily member 15
, vascular endothelial growth inhibitor
, tocopherol (alpha) transfer protein-like
, TNF ligand-related molecule 1
, TNF superfamily ligand TL1A
, vascular endothelial cell growth inhibitor
, vascular endothelial growth inhibitor-192A
, bM20K13.3 (tumor necrosis factor (ligand) superfamily, member 15)