| First Author | Ohashi K | Year | 2000 |
| Journal | J Immunol | Volume | 164 |
| Issue | 2 | Pages | 558-61 |
| PubMed ID | 10623794 | Mgi Jnum | J:59296 |
| Mgi Id | MGI:1351361 | Doi | 10.4049/jimmunol.164.2.558 |
| Citation | Ohashi K, et al. (2000) Cutting edge: heat shock protein 60 is a putative endogenous ligand of the toll-like receptor-4 complex. J Immunol 164(2):558-61 |
| abstractText | 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. |
