Actions of immune cells in the hypertensive kidney

Inflammatory processes play a critical role in the pathogenesis of hypertension. Innate and adaptive immune responses participate in blood pressure (BP) elevation and end-organ damage. In this review, we discuss recent studies illustrating mechanisms through which immune cells and cytokines regulate BP via their actions in the kidney.

Cells of the innate immune system, including monocytes, neutrophils, and dendritic cells, can all promote BP elevation via effects on kidney function. These innate immune cells can directly impact oxidative stress and cytokine generation in the kidney and/or present antigens to lymphocytes for the engagement of the adaptive immune system. Once activated by dendritic cells, effector memory T cells accumulate in the hypertensive kidney and facilitate renal salt and water retention. Individual subsets of activated T cells can secrete tumor necrosis factor-alpha (TNF-α), interleukin-17a (IL-17a), and interferon-gamma (IFN-γ), each of which has augmented the elevation of blood pressure in hypertensive models by enhancing renal sodium transport. B cells, regulate blood pressure via vasopressin receptor 2 (V2R)-dependent effects on fluid transport in the kidney.

Immune cells of the innate and adaptive immune systems drive sodium retention and blood pressure elevation in part by altering renal solute transport.