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J Immunol. 2000 Jan 15;164(2):558-61.

Cutting edge: heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex.

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1
German Diabetes Research Institute, Heinrich-Heine-University, Düsseldorf, Germany.

Abstract

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.

PMID:
10623794
[Indexed for MEDLINE]
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