作者
Daniel W Trott, Salim R Thabet, Annet Kirabo, Mohamed A Saleh, Hana Itani, Allison E Norlander, Jing Wu, Anna Goldstein, William J Arendshorst, Meena S Madhur, Wei Chen, Chung-I Li, Yu Shyr, David G Harrison
发表日期
2014/11
期刊
Hypertension
卷号
64
期号
5
页码范围
1108-1115
出版商
Lippincott Williams & Wilkins
简介
Recent studies have emphasized a role of adaptive immunity, and particularly T cells, in the genesis of hypertension. We sought to determine the T-cell subtypes that contribute to hypertension and renal inflammation in angiotensin II–induced hypertension. Using T-cell receptor spectratyping to examine T-cell receptor usage, we demonstrated that CD8+ cells, but not CD4+ cells, in the kidney exhibited altered T-cell receptor transcript lengths in Vβ3, 8.1, and 17 families in response to angiotensin II–induced hypertension. Clonality was not observed in other organs. The hypertension caused by angiotensin II in CD4−/− and MHCII−/− mice was similar to that observed in wild-type mice, whereas CD8−/− mice and OT1xRAG-1−/− mice, which have only 1 T-cell receptor, exhibited a blunted hypertensive response to angiotensin II. Adoptive transfer of pan T cells and CD8+ T cells but not CD4+/CD25 cells conferred …
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