Figure 1: Chow-fed aMHCII−/− mice reveal adipocyte-specific MHCII deficiency. | Nature Communications

Figure 1: Chow-fed aMHCII−/− mice reveal adipocyte-specific MHCII deficiency.

From: Adipocyte adaptive immunity mediates diet-induced adipose inflammation and insulin resistance by decreasing adipose Treg cells

Figure 1

(a) Adipocyte-specific gene knockout strategy where triangles designate LoxP sites flanking exon1 (EX1) of H2-Ab1. (b) PCR genotyping approach. H2-Ab1 mRNA expression in c tissues (N=6 per group) and (d) cell types (adipocytes, SVF, BMDMs, DCs and PMs, see text) of wild-type (WT; H2-Ab1fl/fl) and aMHCII−/− (KO) mice fed standard chow diet (N=4 per group). (e) H2-Ab1 protein expression in adipocytes and SVF of WT and KO mice fed HFD measured by Western blot. (f) MHCII APC activity of highly-purified adipocytes from chow-fed WT and aMHCII−/− mice (N=3 per group). (g) Body mass and adiposity (N=22–23 per group) and (h) intraperitoneal insulin tolerance test and area under the curve data (N=10–14 per group) of chow-fed WT and aMHCII−/− mice. (i) Flow cytometry analysis of CD4+, CD8+, Treg+ and Th1, and Th2 in eWAT SVF from chow-fed WT and aMHCII−/− mice (N=3–4 per group). Mean±s.e.m.; *P<0.05 or +P<0.1 versus WT by t-test.

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