| First Author | Cohen-Sfady M | Year | 2009 |
| Journal | J Immunol | Volume | 183 |
| Issue | 2 | Pages | 890-6 |
| PubMed ID | 19561102 | Mgi Jnum | J:151657 |
| Mgi Id | MGI:4354697 | Doi | 10.4049/jimmunol.0804238 |
| Citation | Cohen-Sfady M, et al. (2009) Heat shock protein 60, via MyD88 innate signaling, protects B cells from apoptosis, spontaneous and induced. J Immunol 183(2):890-6 |
| abstractText | We recently reported that heat shock protein 60 (HSP60) via TLR4 signaling activates B cells and induces them to proliferate and secrete IL-10. We now report that HSP60 inhibits mouse B cell apoptosis, spontaneous or induced by dexamethasone or anti-IgM activation. Unlike HSP60 enhancement of B cell proliferation and IL-10 secretion, TLR4 signaling was not required for the inhibition of apoptosis by HSP60; nevertheless, MyD88 was essential. Inhibition of apoptosis by HSP60 was associated with up-regulation of the antiapoptotic molecules Bcl-2, Bcl-x(L), and survivin, maintenance of the mitochondrial transmembrane potential, and inhibition of caspase-3 activation. Moreover, B cells incubated with HSP60 manifested prolonged survival following transfer into recipient mice. These results extend the varied role of HSP60 in the innate regulation of the adaptive immune response. |
