Extended Data Fig. 4: Effects of genetic deficiency and blocking of integrin β7 on atherosclerosis.
From: Gut intraepithelial T cells calibrate metabolism and accelerate cardiovascular disease
a, Body weights, cumulative food intake and energy expenditure were measured in Ldlr−/− mice and β7−/−Ldlr−/− mice. n = 4 mice per group. b, Ldlr−/− mice and β7−/−Ldlr−/− mice were fed a HCD for 14 weeks. Plasma cholesterol levels were determined in overnight-fasted mice. n = 7 Ldlr−/− mice; n = 5 β7−/−Ldlr−/− mice; **P < 0.01, two-tailed Mann–Whitney U-test. c, Representative oil-red O images and quantification of plaque size in the aortic roots. n = 7 Ldlr−/− mice; n = 5 β7−/−Ldlr−/− mice; *P < 0.05, two-tailed Mann–Whitney U-test. d, Quantification of Ly-6Chigh monocytes, neutrophils and macrophages in plaques. n = 7 mice per group. *P < 0.05, **P < 0.01, two-tailed Mann–Whitney U-test. e, Ldlr−/− mice that were fed a HCD were treated with anti-integrin β7 antibodies or IgG isotype control (500 μg per mouse per week) for 14 weeks. Mice were subjected to a glucose-tolerance test after 8 weeks on the HCD. n = 6 mice per group; **P < 0.01, two-tailed Mann–Whitney U-test. f, Representative images of oil-red O-stained aortic cross-sections and quantification of plaque size in the aortic roots after 14 weeks on a HCD. n = 5 mice treated with IgG; n = 6 mice treated with anti-integrin β7 antibody; *P < 0.05, **P < 0.01, two-tailed Mann–Whitney U-test. Data are mean ± s.e.m.
