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Cutting Edge: Heat Shock Protein 60 Is a Putative Endogenous Ligand of the Toll-Like Receptor-4 Complex
Open accessAbstract
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-α 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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Metadata
- Authors
- Ohashi, K., Burkart, V., Flohé, S., & Kolb, H.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2000-01
- Volume
- 164
- Issue
- 2
- Pages
- 558-561
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1591714343
- Cited by
- 1,606
- References
- 0
- FWCI
- 31.95
- Type
- journal article
- Language
- en
- Open access
- bronze
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