Renal Effects of Cytokines in Hypertension.

Journal Article (Journal Article;Review)

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.

Full Text

Duke Authors

Cited Authors

  • Wen, Y; Crowley, SD

Published Date

  • 2019

Published In

Volume / Issue

  • 1165 /

Start / End Page

  • 443 - 454

PubMed ID

  • 31399978

International Standard Serial Number (ISSN)

  • 0065-2598

Digital Object Identifier (DOI)

  • 10.1007/978-981-13-8871-2_21


  • eng

Conference Location

  • United States