期刊
INTERNATIONAL JOURNAL OF HYPERTENSION
卷 2014, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2014/126365
关键词
-
资金
- NIH [R01HL105280]
- Steinbronn Heart Failure Research Award
Adaptive immune function is implicated in the pathogenesis of vascular disease. Inhibition of T-lymphocyte function has been shown to reduce hypertension, target-organ damage, and vascular stiffness. To study the role of immune inhibitory cells, CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs), on vascular stiffness, we stimulated the proliferation of Treg lymphocytes in vivo using a novel cytokine immune complex of Interleukin-2 (IL-2) and anti-IL-2 monoclonal antibody clone JES6-1 (mAb(CD25)). Three-month-old male C57BL/6J mice were treated with IL-2/mAb(CD25) concomitantly with continuous infusion of angiotensin type 1 receptor agonist, [Val(5)] angiotensin II. Our results indicate that the IL-2/mAb(CD25) complex effectively induced Treg phenotype expansion by 5-fold in the spleens with minimal effects on total CD4(+) and CD8(+) T-lymphocyte numbers. The IL-2/mAb(CD25) complex inhibited angiotensin II-mediated aortic collagen remodeling and the resulting stiffening, analyzed with in vivo pulse wave velocity and effective Young's modulus. Furthermore, the IL-2/mAb(CD25) complex suppressed angiotensin II-mediated Th17 responses in the lymphoid organs and reduced gene expression of IL-17 as well as T cell and macrophage infiltrates in the aortic tissue. This study provides data that support the protective roles of Tregs in vascular stiffening and highlights the use of the IL2/mAb(CD25) complex as a new potential therapy in angiotensin II-related vascular diseases.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据