• Mao Yang, Simeng Tian, Zhoujun Lin, Zhenkun Fu, and Chenggang Li.
• Department of Cardiology, Electrophysiological Center of Cardiology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
• Medicine (Baltimore). 2022 Nov 11; 101 (45): e31667e31667.

AbstractAccumulating evidence supports the active involvement of vascular inflammation in atherosclerosis pathogenesis. Vascular inflammatory events within atherosclerotic plaques are predominated by innate antigen-presenting cells (APCs), including dendritic cells, macrophages, and adaptive immune cells such as T lymphocytes. The interaction between APCs and T cells is essential for the initiation and progression of vascular inflammation during atherosclerosis formation. B7-CD28 family members that provide either costimulatory or coinhibitory signals to T cells are important mediators of the cross-talk between APCs and T cells. The balance of different functional members of the B7-CD28 family shapes T cell responses during inflammation. Recent studies from both mouse and preclinical models have shown that targeting costimulatory molecules on APCs and T cells may be effective in treating vascular inflammatory diseases, especially atherosclerosis. In this review, we summarize recent advances in understanding how APC and T cells are involved in the pathogenesis of atherosclerosis by focusing on B7-CD28 family members and provide insight into the immunotherapeutic potential of targeting B7-CD28 family members in atherosclerosis.Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.

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