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. Author manuscript; available in PMC: 2019 Oct 26.
Published in final edited form as: Circ Res. 2018 Oct 26;123(10):1118–1120. doi: 10.1161/CIRCRESAHA.118.313816

Figure. Adaptive immune responses in atherosclerosis.

Figure.

Top: In healthy individuals, LDLR on antigen presenting cells (APCs) recognizes and takes up LDL, inducing production of anti-inflammatory cytokines. Self-reactive Tregs recognize ApoB peptides presented by MHC-II on APCs in the context of co-stimulatory molecules that promote Tregs, which also produce anti-inflammatory cytokines production, thereby preventing or dampening atherosclerosis.

Bottom: Modified and oxidized (ox)LDL accumulates in atherosclerotic lesions and is recognized by receptors like TLR14 and CD36 to induce transcription of inflammatory cytokines like IL-12 and IL-23. CD4 T cells recognize ApoB peptides in the context of pro-inflammatory cytokines and strong costimulation, which induces Th1 (T-bet+) and Th17 (RORγt+) T cells. Their production of IFN-γ and IL-17 exacerbates atherosclerosis. Now, CD8 T cells also recognize ApoB epitopes presented by MHC-I and exacerbate inflammation by producing IFN-γ. TCR: T cell receptor, TLR4: toll-like receptor 4.