Hui Pi ¹ Guangliang Wang ² Yu Wang ^2* Ming Zhang ² Qin He ^2* Xilong Zheng ³ Kai Yin ^4* Guojun Zhao ² Ting Jiang ^2*

• ¹ School of Basic Medical Sciences, Dali University, Dali, China
• ² Affiliated Qingyuan Hospital, Guangzhou Medical University, Qingyuan, China
• ³ Departments of Biochemistry and Molecular Biology and Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary Ribbon, Canada
• ⁴ Department of General Practice, The Fifth Affiliated Hospital of Southern Medical University, Guangzhou, China

Atherosclerosis serves as the primary catalyst for numerous cardiovascular diseases.Growing evidence suggests that the immune response is involved in every stage of atherosclerotic plaque evolution. Rapid, but not specific, innate immune arms, including neutrophils, monocytes/macrophages, dendritic cells (DCs) and other innate immune cells, as well as pattern-recognition receptors and various inflammatory mediators, contribute to atherogenesis. The specific adaptive immune response, governed by T cells and B cells, antibodies, and immunomodulatory cytokines potently regulates disease activity and progression. In the inflammatory microenvironment, the heterogeneity of leukocyte subpopulations plays a very important regulatory role in plaque evolution. With advances in experimental techniques, the fine mechanisms of immune system involvement in atherosclerotic plaque evolution are becoming known. In this review, we examine the critical immune responses involved in atherosclerotic plaque evolution, in particular, looking at atherosclerosis from the perspective of evolutionary immunobiology. A comprehensive understanding of the interplay between plaque evolution and plaque immunity provides clues for strategically combating atherosclerosis.