CD11b regulates obesity-induced insulin resistance via limiting alternative activation and proliferation of adipose tissue macrophages

Chunxing Zheng, Qian Yang, Chunliang Xu, Peishun Shou, Jianchang Cao, Menghui Jiang, Qing Chen, Gang Cao, Yanyan Han, Fengying Li, Wei Cao, Liying Zhang, Li Zhang, Yufang Shi, Ying Wang

Research output: Contribution to journalArticle

30 Scopus citations


Obesity-associated inflammation is accompanied by the accumulation of adipose tissue macrophages (ATMs), which is believed to predispose obese individuals to insulin resistance. CD11b (integrin αM) is highly expressed on monocytes and macrophages and is critical for their migration and function. We found here that high-fat diet-induced insulin resistance was significantly reduced in CD11bdeficient mice. Interestingly, the recruitment of monocytes to adipose tissue is impaired when CD11b is deficient, although the cellularity of ATMs in CD11b-deficient mice is higher than that in wild-type mice. We further found that the increase in ATMs is caused mainly by their vigorous proliferation in the absence of CD11b. Moreover, the proliferation and alternative activation of ATMs are regulated by the IL-4/STAT6 axis, which is inhibited by CD11b through the activity of phosphatase SHP-1. Thus, CD11b plays a critical role in obesity-induced insulin resistance by limiting the proliferation and alternative activation of ATMs.

Original languageEnglish (US)
Pages (from-to)E7239-E7248
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number52
StatePublished - Dec 29 2015



  • Alternative activation
  • Insulin resistance
  • Integrin CD11b
  • Macrophage proliferation
  • Obesity

ASJC Scopus subject areas

  • General

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