Cutting Edge: Heat Shock Protein 60 Is a Putative Endogenous Ligand of the Toll-Like Receptor-4 Complex | Zendy

Koji Ohashi | Zendy; Volker Burkart | Zendy; Stefanie B. Flohé | Zendy; Hubert Kolb | Zendy

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Cutting Edge: Heat Shock Protein 60 Is a Putative Endogenous Ligand of the Toll-Like Receptor-4 Complex

Author(s) -

Koji Ohashi,

Volker Burkart,

Stefanie B. Flohé,

Hubert Kolb

Publication year - 2000

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.164.2.558

Subject(s) - tlr4 , toll like receptor , hsp60 , receptor , microbiology and biotechnology , endogeny , proinflammatory cytokine , innate immune system , heat shock protein , biology , ligand (biochemistry) , signal transduction , immunology , inflammation , gene , hsp70 , genetics , biochemistry

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.

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