Adipose Tissue Macrophages Function as Antigen Presenting Cells and Regulate Adipose Tissue CD4+ T Cells in Mice

  1. Carey N. Lumeng1,3,4
  1. 1Department of Pediatrics and Communicable Diseases, University of Michigan Health System, Ann Arbor, MI, USA.
  2. 2Literature, Science and Arts Program, University of Michigan, Ann Arbor, MI, USA.
  3. 3Cellular and Molecular Biology Graduate Program, University of Michigan Medical School, Ann Arbor, MI, USA.
  4. 4Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, USA.
  1. Corresponding Author: Carey N. Lumeng, Email: clumeng{at}umich.edu
  • * Current Address: Indiana University School of Medicine 635 Barnhill Drive, MS 2031A Indianapolis, IN 46202

Abstract

The pro-inflammatory activation of leukocytes in adipose tissue contributes to metabolic disease. How crosstalk between immune cells initiates and sustains adipose tissue inflammation remains an unresolved question. We have examined the hypothesis that adipose tissue macrophages (ATMs) interact with and regulate the function of T cells. Dietary obesity was shown to activate the proliferation of effector memory CD4+ T cells in adipose tissue. Our studies further demonstrate that ATMs are functional antigen presenting cells that promote the proliferation of IFN-γ producing CD4+ T cells in adipose tissue. ATMs from both lean and obese visceral fat process and present MHC class II-restricted antigens. ATMs were sufficient to promote proliferation and IFN-γ production from antigen-specific CD4+ T cells in vitro and in vivo. Diet-induced obesity increased the expression of MHC II and T cell costimulatory molecules on ATMs in visceral fat, which correlated with an induction of T cell proliferation in that depot. Collectively, these data indicate that ATMs provide a functional link between the innate and adaptive immune systems within visceral fat in mice.

Footnotes

    • Received October 9, 2012.
    • Accepted February 27, 2013.

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