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. 2020 Aug 17;8(2):e000964. doi: 10.1136/jitc-2020-000964

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© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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Programmed death-ligand 1 (PD-L1) deletion exacerbates obesity-associated inflammation and metabolic distress. (A) Body weight of wild-type (WT)/knockout (KO) mice given low-fat diet (LFD) or high-fat diet (HFD). (B) Insulin tolerance in obese WT/KO mice. (C) Glucose tolerance. (D) Representative flow cytometry data for CD11b^hiF4/80^hi macrophage population in obese WT/KO visceral white adipose tissue (vWAT). (E) Macrophage prevalence in obese WT/KO vWAT. (F) Prevalence of CD11c⁺ and (G) CD301⁺ percentage of total macrophages. (H) Representative F4/80 immunohistochemistry (IHC). (I) Quantification of relative F4/80 IHC signals. WT level is set as “1.” (J) Representative liver H&E staining. (K) Quantification of liver steatosis area as percentage of the entire liver tissue.