Heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex
Heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex
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DOI：
10.4049/jimmunol.164.2.558
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发表时间：
2000-01-15
影响因子：
4.4
通讯作者：
Kolb, H
中科院分区：
文献类型：
--
作者：
Ohashi, K;Burkart, V;Kolb, H
人热休克蛋白60（hsp 60）在先天免疫系统的细胞中引起强有力的促炎反应，因此被认为是应激或损伤细胞的危险信号。我们在此报告了携带突变型Toll样受体（Tlr）4的C3 H/HeJ小鼠的巨噬细胞对hsp 60无反应。发现TNF-α和NO形成的诱导都依赖于功能性Tlr 4，而CpG DNA对巨噬细胞的刺激不依赖于Tlr 4。我们的结论是，Tlr 4介导热休克蛋白60信号。这是第一个报告的假定内源性配体的Tlr 4复合物。
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.