T Cell-Derived IL-17A Induces Vascular Dysfunction via Perivascular Fibrosis Formation and Dysregulation of ^·NO/cGMP Signaling.

ABSTRACT:

Aims

The neutrophil recruiting cytokine Interleukin-17A (IL-17A) is a key component in vascular dysfunction and arterial hypertension. Moreover, IL-17A has a central role for the vascular infiltration of myeloid cells into the arterial wall in Angiotensin II-induced vascular inflammation. The intention of our study was to analyze the impact of T cell-derived IL-17A on hypertension, vascular function, and inflammation.

Methods and results

Chronic IL-17A overexpression in T cells (CD4-IL-17A^ind/+ mice) resulted in elevated reactive oxygen species in the peripheral blood and a significant vascular dysfunction compared to control mice. The vascular dysfunction seen in the CD4-IL-17A^ind/+ mice was only accompanied by a modest and nonsignificant accumulation

SUBMITTER: Schuler R 

PROVIDER: S-EPMC6668561 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature