Heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex

被引：1253
|
作者：
Ohashi, K [1 ]
Burkart, V [1 ]
Flohé, S [1 ]
Kolb, H [1 ]
机构：
[1] Univ Dusseldorf, German Diabet Res Inst, D-40225 Dusseldorf, Germany
来源：
JOURNAL OF IMMUNOLOGY | 2000年 / 164卷 / 02期
关键词：
D O I：
10.4049/jimmunol.164.2.558
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
Human heat shock protein 60 (hsp60) elicits a potent proinflammatory response in cells of the innate immune system and therefore has been proposed as a danger signal of stressed or damaged cells, We report here that macrophages of C3H/HeJ mice, carrying a mutant Toll-like-receptor (Tlr) 4 are nonresponsive to hsp60. Both the induction of TNF-alpha and NO formation were found dependent on a functional Tlr4 whereas stimulation of macrophages by CpG DNA was Tlr4 independent. We conclude that Tlr4 mediates hsp60 signaling. This is the first report of a putative endogenous ligand of the Tlr4 complex.
引用
收藏
页码：558 / 561
页数：4
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