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Renal Effects of Cytokines in Hypertension

  • Yi Wen
  • Steven D. CrowleyEmail author
Chapter
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1165)

Abstract

Preclinical studies point to a key role for immune cells in hypertension via augmenting renal injury and/or hypertensive responses. Blood pressure elevation in rheumatologic patients is attenuated by anti-inflammatory therapies. Both the innate and adaptive immune systems contribute to the pathogenesis of hypertension by modulating renal sodium balance, blood flow, and functions of the vasculature and epithelial cells in the kidney. Monocytes/macrophages and T lymphocytes are pivotal mediators of hypertensive responses, while dendritic cells and B lymphocytes can regulate blood pressure indirectly by promoting T lymphocytes activation. Pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF), interleukin-1 (IL-1), interleukin-17 (IL-17), and interferon-γ (IFN), amplify blood pressure elevation and/or renal injury. By contrast, interleukin-10 (IL-10) protects against renal and vascular function when produced by T helper 2 cells (Th2) and regulatory T cells (Treg). Thus, understanding the renal effects of cytokines in hypertension will provide targets for precise immunotherapies to inhibit targeted organ damage while preserving necessary immunity.

Keywords

Immune system Cytokine Chemokines Kidney Hypertension 

Notes

Acknowledgements

NIH grants DK087893, HL128355; Veterans Health Administration, Office of Research and Development, Biomedical Laboratory Research and Development Grant BX000893.

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© Springer Nature Singapore Pte Ltd. 2019

Authors and Affiliations

  1. 1.Division of Nephrology, Zhongda HospitalSoutheast UniversityNanjingChina
  2. 2.Division of Nephrology, Department of MedicineDuke University and Durham VA Medical CentersDurhamUSA

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