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: Chemokines; Cytokine; Hypertension; Immune system; Kidney.