Extended Data Fig. 5: Analysis of CCR8 transcript expression across tissues and cell types and consequences of CCR8 blocking.
(a) CCR8 mRNA expression in different tissues of consensus datasets from The Human Protein Atlas. Tissues of the same system (nervous system, endocrine system, digestion system, etc.) are depicted in the same color; (b) CCR8 mRNA expression in different blood cell types of consensus datasets from The Human Protein Atlas; (c) Ccr8 mRNA expression in different T cell populations of the para-aortic LNs from Apoe−/−Ccl17e/wt and Apoe−/−Ccl17e/e mice fed a WD for 6 weeks; (d) Flow cytometric quantification of CCR8 expression on DCs from LN of the indicated mouse strains (n = 5 per strain); (e) CCL3 titers in supernatants of CD4+ T cells from Apoe−/− mice stimulated with CCL17 or vehicle for 4 hours in the presence or absence of an antibody to CCR8 (number of replicates in parentheses over number of independent experiments per bar from left to right: n = 8, 8, 7, 7); (f) Experimental scheme of Apoe−/− mice injected with isotype control or CCR8-blocking antibody during WD feeding for 4 weeks. (g-i) Quantification of the percentage of lesional Mac2+ macrophages (g, isotype, n = 9; anti-CCR8, n = 5), SMA+ SMCs (h, isotype, n = 9; anti-CCR8, n = 6) and collagen content (i, isotype, n = 10; anti-CCR8, n = 5) of Apoe−/− mice receiving an isotype or CCR8 blocking antibody during WD feeding for 4 weeks. (a-i) Data represent mean ± SEM. Two-sided P values as indicated and analyzed by Mann-Whitney U-test or unpaired Student’s t-test (c, g-i) or two-way ANOVA with Holm-Å Ãdák’s post hoc test (e).
