Journal
CELL REPORTS
Volume 9, Issue 2, Pages 605-617Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2014.09.004
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Funding
- NIH/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [DK090262, DK092873, DK095050, DK097449]
- American Diabetes Association [07-12-CD-08]
- NIH National Institute of Allergy and Infectious Diseases Experimental Training in Immunology [T32 AI007413-19]
- NIH NIDDK [F32 DK091976]
- NIH Minority Training Supplement [DK090262-S1]
- NIH [DK089503]
- NIH from the NIDDK [2P30-DK20572]
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An adaptive immune response triggered by obesity is characterized by the activation of adipose tissue CD4(+) T cells by unclear mechanisms. We have examined whether interactions between adipose tissue macrophages (ATMs) and CD4(+) T cells contribute to adipose tissue metainflammation. Intravital microscopy identifies dynamic antigen-dependent interactions between ATMs and T cells in visceral fat. Mice deficient in major histocompatibility complex class II (MHC II) showed protection from diet-induced obesity. Deletion of MHC II expression in macrophages led to an adipose tissue-specific decrease in the effector/memory CD4(+) T cells, attenuation of CD11c(+) ATM accumulation, and improvement in glucose intolerance by increasing adipose tissue insulin sensitivity. Ablation experiments demonstrated that the maintenance of proliferating conventional T cells is dependent on signals from CD11c(+) ATMs in obese mice. These studies demonstrate the importance of MHCII-restricted signals from ATMs that regulate adipose tissue T cell maturation and metainflammation.
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