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Part of the book series: Heat Shock Proteins ((HESP,volume 1))

Abstract

Heat shock protein (HSP) 60 functions as a key signal to the immune system: its expression is up-regulated under inflammation and HSP60-reactive T and B cells were observed in almost all inflammatory diseases. Moreover, HSP60 induces pro-inflammatory phenotype in innate immune cells via Toll-like receptors (TLRs). Accordingly, HSP60 has been considered a pro-inflammatory “danger signal”. However, HSP60 have immunoregulatory potential and could arrest inflammatory damage. In this chapter we discuss recent findings indicating that T and B cells may directly respond to HSP60 via TLR-2 and TLR4 respectively. HSP60 inhibits T-cell chemotaxis, shift the cytokine secretion balance towards a Th2 phenotype, and activates the suppression ability of Treg. B cells responding to HSP60 secreted also high levels of IL-10. Then, these innate effects of HSP60 on adaptive immune system lead to resolution of inflammation. Thus, HSP60, which is up-regulated by stress and inflammation, can innately resolve it

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Zanin-Zhorov, A., Cohen, I.R. (2007). HSP60: A Pleiotropic Immune Signal. In: Asea, A.A., Maio, A.D. (eds) Heat Shock Proteins: Potent Mediators of Inflammation and Immunity. Heat Shock Proteins, vol 1. Springer, Dordrecht. https://doi.org/10.1007/978-1-4020-5585-0_16

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