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

Author

Listed:
  • Yunmeng Liu

    (University of Arkansas for Medical Sciences)

  • Tonya M. Rafferty

    (University of Arkansas for Medical Sciences
    Present address: Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, USA)

  • 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
    Present address: State Key Laboratory of Cardiovascular Disease, FuWai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China)

  • Benjamin Ko

    (University of Chicago)

  • Robert S. Hoover

    (Emory University
    Research Service Atlanta, Veteran’s Administration Medical Center)

  • Beixiang He

    (University of Arkansas for Medical Sciences
    University of Arkansas for Medical Sciences)

  • Shengyu Mu

    (University of Arkansas for Medical Sciences)

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.

Suggested Citation

  • Yunmeng Liu & Tonya M. Rafferty & Sung W. Rhee & Jessica S. Webber & Li Song & Benjamin Ko & Robert S. Hoover & Beixiang He & Shengyu Mu, 2017. "CD8+ T cells stimulate Na-Cl co-transporter NCC in distal convoluted tubules leading to salt-sensitive hypertension," Nature Communications, Nature, vol. 8(1), pages 1-14, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14037
    DOI: 10.1038/ncomms14037
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