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TNF/Lymphotoxin alpha/beta deficiency influences PM2.5 exposure-induced response of energy metabolism through alterations in both food intake and energy expenditure.
The expression of lymphotoxin (LT)-B was significantly downregulated in the absence of T cells from nude mice and was recovered after the transfusion of T cells.
Expression of LT alpha (show LTA ELISA Kits) and beta on acinar cells in mice led to chronic pancreatitis and sufficed to reproduce key features of human autoimmune pancreatitis including the development of autoimmunity and AIP (show AIP ELISA Kits) associated secondary extra pancreatic pathologies.
TNF (show TNF ELISA Kits) is able to upregulate LT-beta expression in hepatic cells at the transcriptional level by the binding of NF-kappaB p50 (show NFKB1 ELISA Kits)/p65 (show NFkBP65 ELISA Kits) heterodimers and Ets1 (show ETS1 ELISA Kits) to their respective sites in the LT-beta promoter.
LTbeta RNA is detectable in embryos ranging from 5.5 to 18.5 days of development, e.g., in peripheral lymph nodes, Peyer's patches, thymus and skin of the E18.5 embryo and fetal liver of E12.5.
membrane lymphotoxin beta contributes to anti-leishmanial immunity by controlling structural integrity of lymphoid organs
The organogenic function of B-LTbeta is almost entirely restricted to spleen, where it supports the correct lymphoid architecture that is critical for an effective humoral immune response.
microenvironment in peripheral lymphoid organs associated with lymphotoxin alpha (show LTA ELISA Kits)/lymphotoxin beta-lymphotoxin beta receptor (show LTBR ELISA Kits) signaling and chemokine (show CCL1 ELISA Kits) production is critical for recruitment efficiency of dendritic cel
membrane LT-beta is important in resistance to Theiler's virus infection
Lymphotoxin-mediated adhesion molecule (show NCAM1 ELISA Kits) expression may be important in the development of graft-versus-host skin disease.
TNF (show TNF ELISA Kits) is able to upregulate LT-beta expression in hepatic cells at the transcriptional level by the binding of NF-kappaB p50 (show NFKB1 ELISA Kits)/p65 (show GORASP1 ELISA Kits) heterodimers and Ets1 (show ETS1 ELISA Kits) to their respective sites in the LT-beta promoter.
The multifaceted character of lymphotoxin beta may be involved in inflammatory myopathies and muscular dystrophies.
A strong association was found between several single nucleotide polymorphisms in the LTA (show LTA ELISA Kits)/LTB/TNFalpha (show TNF ELISA Kits) locus and Sjogren syndrome.
Data show differential expression of interferon-gamma (show IFNG ELISA Kits), TNFSF3, TNFSF10 (show TNFSF10 ELISA Kits), TNFSF12 (show TNFSF12 ELISA Kits) and PDGFbeta in CD8 (show CD8A ELISA Kits)+, CD14 (show NDUFA2 ELISA Kits)+ and CD4 (show CD4 ELISA Kits)+ cells.
Findings provide evidence of additional complexity in the transcriptional regulation of LTB with implications for coordinate expression of genes in this important genomic locus.
Heterotypic interaction between LTbeta-producing lymphocytes and responding fibroblast-like synoviocytes contributes to establishment of complex lymphoid microstructures. May be one element in susceptibility of synovial membrane to lymphoid organogenesis.
The identification of IL-6 (show IL6 ELISA Kits) and IL-1beta (show IL1B ELISA Kits) as activators of LT-beta supports their involvement in LT-beta signaling in liver regeneration associated with chronic liver damage.
Lymphotoxin (LT) beta receptor ligands LTalpha1 and -beta2 activate both the classical and noncanonical NF-kappa B (show NFKB1 ELISA Kits) pathways in human vascular endothelial cells and dermal microvascular endothelial cells in vitro.
LT-Beta may play a role in rheumatoid arthritis disease pathogenesis by contributing to a more intense inflammatory reaction in the synovium
blocking the lymphotoxin-beta receptor (show LTBR ELISA Kits) pathway results in ablation of the lymphoid organization in the NOD salivary glands and thus an improvement in salivary gland function.
These results suggest that colonization by commensal bacteria may affect the maturation of neonatal ileal Pps (show IRF6 ELISA Kits) by the induction of LT-beta via toll (show TLR4 ELISA Kits)-like receptors.
Lymphotoxin beta is a type II membrane protein of the TNF family. It anchors lymphotoxin-alpha to the cell surface through heterotrimer formation. The predominant form on the lymphocyte surface is the lymphotoxin-alpha 1/beta 2 complex (e.g. 1 molecule alpha/2 molecules beta) and this complex is the primary ligand for the lymphotoxin-beta receptor. The minor complex is lymphotoxin-alpha 2/beta 1. LTB is an inducer of the inflammatory response system and involved in normal development of lymphoid tissue. Lymphotoxin-beta isoform b is unable to complex with lymphotoxin-alpha suggesting a function for lymphotoxin-beta which is independent of lympyhotoxin-alpha. Alternative splicing results in multiple transcript variants encoding different isoforms.
, lymphotoxin beta
, tumor necrosis factor C
, tumor necrosis factor ligand superfamily member 3
, lymphotoxin B
, Tumor necrosis factor C