Role of interleukin-23/interleukin-17 axis in T-cell-mediated actions in hypertension

被引:36
作者
Higaki, Akinori [1 ]
Mahmoud, Ahmad U. M. [1 ]
Paradis, Pierre [1 ]
Schiffrin, Ernesto L. [1 ,2 ]
机构
[1] McGill Univ, Sir Mortimer B Davis Jewish Gen Hosp, Lady Davis Inst Med Res, 3755 Cote Ste Catherine Rd, Montreal, PQ H3T 1E2, Canada
[2] McGill Univ, Sir Mortimer B Davis Jewish Gen Hosp, Dept Med, 3755 Cote Ste Catherine Rd, Montreal, PQ H3T 1E2, Canada
基金
加拿大健康研究院;
关键词
Interleukin-23; receptor; Adaptive immunity; Immune therapy; GAMMA-DELTA T; II-INDUCED HYPERTENSION; INTERLEUKIN; 17; RENAL INJURY; DOWN-REGULATION; RECEPTOR; IL-17; ACTIVATION; PROMOTES; TH17;
D O I
10.1093/cvr/cvaa257
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Current knowledge suggests that hypertension is in part mediated by immune mechanisms. Both interleukin (IL)-23 and IL-17 are up-regulated in several experimental hypertensive rodent models, as well as in hypertensive humans in observational studies. Recent preclinical studies have shown that either IL-23 or IL-17A treatment induce blood pressure elevation. However, the IL-23/IL-17 axis has not been a major therapeutic target in hypertension, unlike in other autoimmune diseases. In this review, we summarize current knowledge on the role of these cytokines in immune mechanisms contributing to hypertension, and discuss the potential of IL-23/IL-17-targeted therapy for treatment of hypertension. [GRAPHICS] .
引用
收藏
页码:1274 / 1283
页数:10
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