期刊文献+

TLRs及其在痤疮中的作用 被引量:3

下载PDF
导出
摘要 Toll样受体(Toll-like receptors,TLRs)是新近发现的先天免疫的细胞跨膜受体及病原模式识别受体之一,在急性炎症反应中对细胞吞噬的调节,信号的传导及细胞凋亡方面起重要作用。而炎症反应是痤疮发病机制中的重要组成部分。本文对Toll样受体及其在痤疮中的作用进行综述。
出处 《岭南皮肤性病科杂志》 2005年第4期345-347,共3页 Southern China Journal of Dermato-Venereology
  • 相关文献

参考文献20

二级参考文献71

  • 1Hoshino K, Takeuchi O, Kawai T, et al. Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysac-charide: evidence for TLR4 as the Lps gene product. J Immunol,1999,162: 3749-3752.
  • 2Yang RB, Mark MR, Gray A, et al. Toll-like receptor-2 mediates lipopolysaccharide-indueed cellular signalling. Nature, 1998, 395:284-288.
  • 3Kirschning CJ, Wesche H, Merrill Ayres T, et al. Human toll-like receptor 2 confers responsiveness to bacterial lipopolysaccharide. J Exp Med, 1998,188:2091-2097.
  • 4Yang RB, Mark MR, Gumey AL, et al. Signaling events induced by lipopolysaccharide-activated toll-like receptor 2. J Immunol,1999,163:639-643.
  • 5Brightbill HD, Library DH, Krutzik SR, et al. Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors.Science, 1999,285 : 732-736.
  • 6Qureshi ST, Iariviere L, Leveque G, et al. Endotoxin-tolerant mice have mutations in Toll-like receptor 4 (TLR4). J Exp Med, 1999,189:615-625.
  • 7Pohorak A, He X, Smimova I, et al. Defective LPS aignaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 geae. Science, 1998,282 : 2085-2088.
  • 8Chow JC, Young DW, Golenbock DT, et al. Toll-like receptor-4 mediates lipopolysaccharide-induced signal transduction. J Biol Chem, 1999,274:10689-10692.
  • 9Shimazu R, Akashi S, Ogata H, etal. MD-2, a molecule that confers lipopolysaccharide responsiveness on Toll-like receptor 4. J Exp Med., 1999,189:1777-1782.
  • 10Ohashi K, Burkart V, Flohe S, et al. Cutting edge: heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex. J Immunol,2000,164:558-561.

共引文献20

同被引文献34

引证文献3

二级引证文献27

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部