Commentary 10.1172/JCI131935

Orai1: CRACing the Th17 response in AKI

Sanjeev Noel

Division of Nephrology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland, USA.

Address correspondence to: Sanjeev Noel, 720 Rutland Avenue, Ross 970, Baltimore, Maryland 21205, USA. Phone: 443.287.2703; Email: snoel6@jhmi.edu.

Find articles by Noel, S. in: JCI | PubMed | Google Scholar |

First published October 14, 2019 - More info

Published in Volume 129, Issue 11 on November 1, 2019
J Clin Invest. 2019;129(11):4583–4586. https://doi.org/10.1172/JCI131935.
© 2019 American Society for Clinical Investigation
First published October 14, 2019 - Version history

A strong Th17 inflammatory response aggravates ischemia reperfusion–induced (IR-induced) acute kidney injury (AKI), tissue fibrosis, and AKI-to–chronic kidney disease (CKD) progression. However, the underlying mechanisms of sustained Th17 activation following AKI and during AKI-to-CKD progression are unclear. In this issue of the JCI, Mehrotra et al. present compelling evidence that the store-operated calcium (Ca2+) channel Orai1 sustains Th17-driven inflammatory response after AKI and drives the AKI-to-CKD transition. Orai1 blockade significantly protected renal function from IR, attenuated high-salt–induced AKI-to-CKD progression in rats, and decreased Th17 response in rat and human T cells. Therapeutic targeting of Orai1 can potentially reduce AKI, AKI-to-CKD progression, and other Th17-driven diseases.

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