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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 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 associated secondary extra pancreatic pathologies.
TNF is able to upregulate LT-beta expression in hepatic cells at the transcriptional level by the binding of NF-kappaB p50/p65 heterodimers and Ets1 to their respective sites in the LT-beta promoter.
Lymphotoxin-beta-receptor (LTbetaR) signaling, a pathway essential for lymphoid organogenesis, abrogates tertiary lymphoid organ development in heart transplantation.
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/lymphotoxin beta-lymphotoxin beta receptor signaling and chemokine production is critical for recruitment efficiency of dendritic cel
role in lymphoid organ neogenesis
membrane LT-beta is important in resistance to Theiler's virus infection
Lymphotoxin-mediated adhesion molecule expression may be important in the development of graft-versus-host skin disease.
Contributes to nasal-associated lymphoid tissue development and function through regulation of lymphoid chemokines and adhesion molecules.
LTbeta, LTbeta receptor, and IFNgamma are involved in oval cell-mediated, but not hepatocyte-mediated, liver regeneration, and the absence of these pathways impairs the oval cell-dependent regenerative response.
The lymphotoxin beta signaling pathway is an essential effector pathway for host defense against the beta-herpesvirus muromegalovirus (MCMV).
Data show that, as an ectodysplasin target, lymphotoxin-beta regulates hair phenotype in developing hair follicles.
Data show that signaling of lymphotoxin (LT) alphabeta through the LTbeta receptor (LTbetaR) is indispensable for regulating peripheral but not thymic Valpha14i NKT cell numbers.
Expression of LTbeta on lymphocytes enhances the induction of immune responses against limiting amounts of antigen
Expression of lymphotoxin-alphabeta on antigen-specific T cells is required for DC function.
Activation of LTbetaR by LTalphabeta mainly expressed on T lymphocytes is crucial for the down regulation of the inflammatory response in this experimental model.
Combination of an EGFR tyrosine kinase inhibitor and a NF-kappaB inhibitor effectively suppressed cetuximab-resistant HNSCC and interfering with the EGFR-LTbeta interaction reverses resistance.
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/LTB/TNFalpha locus and Sjogren syndrome.
Data show differential expression of interferon-gamma, TNFSF3, TNFSF10, TNFSF12 and PDGFbeta in CD8+, CD14+ and CD4+ 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.
Soluble LTalphabeta in synovial fluid is associated with a proinflammatory cytokine milieu that contributes to synovitis in rheumatoid arthritis.
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 and IL-1beta 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 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 pathway results in ablation of the lymphoid organization in the NOD salivary glands and thus an improvement in salivary gland function.
Overexpression of human TNF, lymphotoxin-alpha, and lymphotoxin-beta in mice (transgenic mice) resulted in thymic atropy. Chronic infections may promote thymic atrophy by upregulating lymphotoxin and TNF production.
Sustained LT signaling represents a pathway involved in hepatitis-induced hepatocellular carcinoma.
These results suggest that colonization by commensal bacteria may affect the maturation of neonatal ileal Pps by the induction of LT-beta via toll-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