Inhibition of Interleukin-17A, But Not Interleukin-17F, Signaling Lowers Blood Pressure, and Reduces End-Organ Inflammation in Angiotensin II–Induced Hypertension

Abstract

Inflammatory cytokines play a major role in the pathophysiology of hypertension. The authors previously showed that genetic deletion of interleukin (IL)-17A results in blunted hypertension and reduced renal/vascular dysfunction. With the emergence of a new class of monoclonal antibody–based drugs for psoriasis and related autoimmune disorders that target IL-17 signaling, the authors sought to determine whether these antibodies could also reduce blood pressure, renal/vascular inflammation, and renal injury in a mouse model of hypertension. The authors show that antibodies to IL-17A or the IL-17RA receptor subunit, but not IL-17F, may be a novel adjunct treatment for hypertension and the associated end-organ dysfunction.

Keywords

• angiotensin II
• gamma delta T cells
• hypertension
• interleukin-17A
• interleukin-17F
• interleukin-17RA receptor
• T lymphocytes