Abstract
Currently two mechanisms are recognized by which heat shock proteins (HSP) are released from cells; a passive release mechanism, including necrotic cell death, severe blunt trauma, surgery and following infection with lytic viruses, and an active release mechanism which involves the non classical protein release pathway. HSPs are released both as free HSP and within exosomes. This review covers recent findings on the mechanism by which stress induces the release of HSP72 into the circulation and the biological significance of circulating HSP72 to host defense against disease.
Keywords
Cancer Chaperokine heat shock proteins inflammation receptors signal transductionAbbreviations used
- APC
antigen presenting cells
- eHSP72
extracellular HSP72
- Hsc73
constitutive seventy-kilo Dalton heat shock protein
- HSP72
inducible seventy-kilo Dalton heat shock protein
- IFN-γ
interferon-gamma
- iHSP72
intracellular HSP72
- TLR
toll-like receptors
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