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

被引：1255

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

页码：558 / 561

页数：4

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