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

摘要

class="kwd-title">Key Words: angiotensin II, gamma delta T cells, hypertension, interleukin-17A, interleukin-17F, interleukin-17RA receptor, T lymphocytes class="kwd-title">Abbreviations and Acronyms: Ang II, angiotensin II; ANOVA, analysis of variance; DOCA-salt, deoxycorticosterone acetate and high-salt diet; ELISA, enzyme-linked immunosorbent assay; FDA, Food and Drug Administration; Ig, immunoglobulin; IL, interleukin; IL-17RA, interleukin-17 receptor A; TGF, transforming growth factor class="head no_bottom_margin" id="abs0010title">SummaryInflammatory 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.