
CCR4 수용체의 결핍은 동맥경화증의 초기 발달을 가속화하며, 이는 CCR4가 조절 T 세포의 기능과 이동을 통해 염증 반응을 제어하는 데 중요한 역할을 한다는 것을 시사한다.


coremsg

Chronic inflammation via dysregulation of T cell immune responses is critically involved in the pathogenesis of atherosclerotic cardiovascular disease. Improving the balance between proinflammatory T cells and anti-inflammatory regulatory T cells (Tregs) may be an attractive approach for treating atherosclerosis. Although C-C chemokine receptor 4 (CCR4) has been shown to mediate the recruitment of T cells to inflamed tissues, its role in atherosclerosis is unclear. Here, we show that genetic deletion of CCR4 in hypercholesterolemic mice accelerates the development of early atherosclerotic lesions characterized by an inflammatory plaque phenotype. This was associated with proinflammatory T helper type 1 (Th1) cell-skewed responses in peripheral lymphoid tissues, para-aortic lymph nodes, and atherosclerotic aorta. Mechanistically, CCR4 deficiency in Tregs impaired their suppressive function and migration to the atherosclerotic aorta and augmented Th1 cell-mediated immune responses through defective regulation of dendritic cell function, which accelerated aortic inflammation and atherosclerotic lesion development. Thus, we revealed a previously unrecognized role for CCR4 in controlling the early stage of atherosclerosis via Treg-dependent regulation of proinflammatory T cell responses. Our data suggest that CCR4 is an important negative regulator of atherosclerosis.

### Competing Interest Statement

The authors have declared no competing interest.

C-C chemokine receptor 4 deficiency exacerbates early atherosclerosis in mice

c-c-케모카인-수용체-4-결핍은-생쥐의-초기-동맥경화증을-악화시킨다


C-C 케모카인 수용체 4 결핍은 생쥐의 초기 동맥경화증을 악화시킨다
