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Heat-shock protein-70 and regulatory T cell–mediated protection from ischemic injury
Stephen O'Neill, Jeremy Hughes Kidney International Volume 85, Issue 1, Pages 5-7 (January 2014) DOI: /ki Copyright © 2014 International Society of Nephrology Terms and Conditions
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Figure 1 Heat preconditioning upregulates heat-shock protein-70, leading to regulatory T-cell expansion and recruitment and suppression of inflammation in renal ischemia/reperfusion injury. Schematic diagram illustrating the potential beneficial effects on renal ischemia/reperfusion injury (IRI) of heat-shock protein-70 (HSP70) upregulation induced by either heat preconditioning or pharmacological agents. Induction of HSP70 expression in splenic CD11c+ cells induces expansion of regulatory T cells (Tregs) that ameliorate renal injury, as reported by Kim et al.13 Tregs may also be induced by adenosine 2A receptor (A2AR) agonists. Also, HSP70 induction in renal parenchymal cells such as tubular epithelial cells may exert a protective action by limiting cell death. DCs, dendritic cells; HSF1, heat-shock transcription factor 1; HSP90, heat-shock protein-90; IL-10, interleukin-10; TGF-β, transforming growth factor-β. Kidney International , 5-7DOI: ( /ki ) Copyright © 2014 International Society of Nephrology Terms and Conditions
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