LTBR


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LTBR

A gene on chromosome 12p13 that encodes lymphotoxin beta receptor, which belongs to the tumour-necrosis-factor-receptor superfamily and is expressed on the surface of most cell types (e.g., epithelial and myeloid lineages), but not on T or B cells. LTBR specifically binds the lymphotoxin membrane form (a complex of lymphotoxin-alpha and lymphtoxin-beta) and, with its ligand, plays a role in the development and organisation of lymphoid tissue and transformed cells. LTBR activation can trigger apoptosis; it associates with TRAF3, TRAF4 and TRAF5.
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The epigenetic susceptible candidates including AZU1, LTBR, RTEL1, and VCAM1 were identified as triggers of autoimmune signaling cascades and contributed to derailed pro-/anti-inflammatory cells.
Li et al., "Association of LTBR polymorphisms with chronic hepatitis B virus infection and hepatitis B virus-related hepatocellular carcinoma," International Immunopharmacology, vol.
(b) Curves of DMRs for LTBR. RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; pSS: primary Sjogren's syndrome; HC: healthy controls; IstExon: the first exon zone; TSS: the transcription start site; TSS1500: I500bp upstream of the TSS; TSS200: 200 bp upstream of the TSS.
RT-PCR was performed using Cepheid Smart Cycler (Sunnyvale, CA), Sybergreen Master mix (Qiagen, CA), and gene specific primers for IL-4, LIGHT, LTBR, TSLP, and ADAM-33 (Life Technologies, MD).
Effect of Insulin Infusion on Expression of IL-4, ADAM-33, LIGHT, LTBR, MMP-9, and TSLP.
Our current data also show that there was a concomitant suppression of ADAM-33, LIGHT, and LTBR, three other mediators known to be associated with the pathogenesis of asthma.
LIGHT and its receptor LTBR have very recently been shown to be involved in bronchial remodeling and sensitization to allergens [5].
Furthermore, our recent data show that an injection of 300 mg of hydrocortisone (=60 mg prednisone) suppresses the expression of IL-4, LTBR, ADAM33, and MMP-9 and the plasma concentration of MCP-1.
Since IL-4, LIGHT, LTBR, TGF[beta], MMP-9, and NO are key mediators involved in the pathogenesis of allergy and asthma, the increase in their expression may contribute to the increased vulnerability and risk of asthma in the obese.
[1] Nonstandard abbreviations: TSE, transmissible spongiform encephalopathy; BSE, bovine spongiform encephalopathy; CJD, Creutzfeldt-Jakob disease; CWD, chronic wasting disease; [PrP.sup.C], cellular prion protein; [PrP.sup.Sc], scrapie prion protein; GPI, glycosylphosphatidylinositol; FTIR, Fourier transform infrared; NMR, nuclear magnetic resonance; FDA, Food and Drug Administration; EDRF, erythroid differentiation-related factor; and LTBR, lymphotoxin [beta]-receptor.