Gene expressions of lipopolysaccharide receptors, toll-like receptors 2 and 4, are differently regulated in mouse T lymphocytes.

摘要: Toll-like receptors (TLRs) are a family of mammalian proteins homologous to Drosophila Toll. Human TLR2 was shown mediate the responsiveness lipopolysaccharide (LPS). On other hand, gene mutations mouse TLR4 (mTLR4) in LPS-hyporesponsive strains have suggested that mTLR4 is essential for LPS-signaling mice, but role mTLR2 has not been explored. This report describes molecular cloning cDNA. Overexpression and CD14 conferred LPS-inducibility c-Jun N-terminal kinase phosphorylation nuclear factor-kappaB activation COS7 cells, suggesting signaling receptor LPS. Both genes were expressed T cells. Treatment with anti-CD3epsilon, PMA plus ionomycin, or interleukin-2 (IL-2)/IL-15 increased messenger RNA (mRNA) some cell lines. Specific inhibitors mitogen-activated extracellular signal-regulated fusion protein 38 (p38) inhibited mRNA up-regulation by ionomycin. suggests p38 pathways involved. Additionally, LPS treatment EL-4 line decreased IL-4 expression. Our results indicate both involved signaling, their expressions regulated differently may directly affect T-cell functions binding TLRs. (Blood. 2000;95:1378-1385)