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. Author manuscript; available in PMC: 2021 May 8.
Published in final edited form as: Circ Res. 2020 May 7;126(10):1324–1326. doi: 10.1161/CIRCRESAHA.120.316981

Figure 1.

Figure 1.

Monocyte and macrophage subsets contribute to the initiation, progression, and thrombus formation stages of atherosclerosis. (A) Bone marrow-derived monocytes in circulation are classified as conventional (cMos) and patrolling (pMos) monocytes. During atherogenesis, the Ly6C+ cMos subpopulation infiltrates the intima, whereas the Ly6C- pMos subpopulation secretes inflammatory cytokines while patrolling the endothelium. (B) In the intima, pro-inflammatory macrophages contribute to plaque progression, while anti-inflammatory macrophages aid in plaque regression. (C) In the Roberts et al. study, genetic ablation of Lyn in mice leads to the expansion of pMos subpopulation only. The Lyn-deficient pMos have increased expression of genes that play a role in heat shock protein response, apoptosis inhibition, and innate immunity, compared to WT pMos. The Lyn-deficient mice are also protected against atherosclerosis.