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MGI Accession ID: MGI:4354697
J Number: J:151657
Other Accession IDs: Title: Heat shock protein 60, via MyD88 innate signaling, protects B cells from apoptosis, spontaneous and induced.
Authors: Cohen-Sfady M; Pevsner-Fischer M; Margalit R; Cohen IR
Journal: J Immunol
Volume: 183
Issue: 2
Date: 2009 Jul 15
Year: 2009
Pages: 890-6
Review Status: Peer Reviewed

Abstract:

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.

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