Recent advances on immunity and hypertension: the new cells on the kidney block.

Over the past 50 years, the contribution of the immune system has been identified in the development of hypertension and renal injury. Both human and experimental animal models of hypertension have demonstrated that innate and adaptive immune cells, along with their cytokines and chemokines, modulate blood pressure fluctuations and end organ renal damage. Numerous cell types of the innate immune system, specifically monocytes, macrophages, and dendritic cells, present antigenic peptides to T cells, promoting inflammation and the elevation of blood pressure. These T cells and other adaptive immune cells migrate to vascular and tubular cells of the kidney and promote end-organ fibrosis, damage, and ultimately hypertensive injury. Through the development of high-throughput screening, novel renal and immune cell subsets have been identified as possible contributors and regulators of renal injury and hypertension. In this review, we will consider classical immunological cells and their contribution to renal inflammation, and novel cell subsets, including renal stromal cells, that could potentially shed new light on renal injury and hypertension. Finally, we will discuss how interorgan inflammation contributes to the development of hypertension and hypertension-related multiorgan damage, and explore the clinical implications of the immunological components of renal injury and hypertension.