作者: Ken-ichiro Iwami , Tetsuya Matsuguchi , Akio Masuda , Takeshi Kikuchi , Tipayaratn Musikacharoen
DOI: 10.4049/JIMMUNOL.165.12.6682
关键词:
摘要: Toll-like receptors (TLRs) are a family of proteins playing important roles in host defense. Mice defective functional TLR4 hyporesponsive to LPS, suggesting that is essential for LPS signaling. Here we report the cloning an alternatively spliced mouse (mTLR4) mRNA. The additional exon exists between second and third reported mTLR4 gene contains in-frame stop codon. mRNA encodes 86 aa 36 aa. This expressed partially secretary 20-kDa protein, which named soluble (smTLR4). In macrophage cell line, exogenously smTLR4 significantly inhibited LPS-mediated TNF-alpha production NF-kappaB activation. Additionally, macrophages, increased smTLR4. Taken together, our results indicate may function as feedback mechanism inhibit excessive responses macrophages.