CD8+ T cells stimulate Na-Cl co-transporter NCC in distal convoluted tubules leading to salt-sensitive hypertension

Yunmeng Liu, Tonya M. Rafferty, Sung W. Rhee, Jessica S. Webber, Li Song, Benjamin Ko, Robert S. Hoover, Beixiang He and Shengyu Mu ()
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Yunmeng Liu: University of Arkansas for Medical Sciences
Tonya M. Rafferty: University of Arkansas for Medical Sciences
Sung W. Rhee: University of Arkansas for Medical Sciences
Jessica S. Webber: University of Arkansas for Medical Sciences
Li Song: University of Arkansas for Medical Sciences
Benjamin Ko: University of Chicago
Robert S. Hoover: Emory University
Beixiang He: University of Arkansas for Medical Sciences
Shengyu Mu: University of Arkansas for Medical Sciences

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract Recent studies suggest a role for T lymphocytes in hypertension. However, whether T cells contribute to renal sodium retention and salt-sensitive hypertension is unknown. Here we demonstrate that T cells infiltrate into the kidney of salt-sensitive hypertensive animals. In particular, CD8+ T cells directly contact the distal convoluted tubule (DCT) in the kidneys of DOCA-salt mice and CD8+ T cell-injected mice, leading to up-regulation of the Na-Cl co-transporter NCC, p-NCC and the development of salt-sensitive hypertension. Co-culture with CD8+ T cells upregulates NCC in mouse DCT cells via ROS-induced activation of Src kinase, up-regulation of the K+ channel Kir4.1, and stimulation of the Cl− channel ClC-K. The last event increases chloride efflux, leading to compensatory chloride influx via NCC activation at the cost of increasing sodium retention. Collectively, these findings provide a mechanism for adaptive immunity involvement in the kidney defect in sodium handling and the pathogenesis of salt-sensitive hypertension.

Date: 2017
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DOI: 10.1038/ncomms14037

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