Adipose Tissue Macrophages Function As Antigen-Presenting Cells and Regulate Adipose Tissue CD4+ T Cells in Mice
- David L. Morris1,
- Kae Won Cho1,
- Jennifer L. DelProposto1,
- Kelsie E. Oatmen2,
- Lynn M. Geletka1,
- Gabriel Martinez-Santibanez3,
- Kanakadurga Singer1 and
- Carey N. Lumeng1,3,4⇑
- 1Department of Pediatrics and Communicable Diseases, University of Michigan Health System, Ann Arbor, Michigan
- 2Literature, Science and Arts Program, University of Michigan, Ann Arbor, Michigan
- 3Cellular and Molecular Biology Graduate Program, University of Michigan Medical School, Ann Arbor, Michigan
- 4Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan
- Corresponding author: Carey N. Lumeng, .
The proinflammatory 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 interferon-γ–producing CD4+ T cells in adipose tissue. ATMs from lean and obese visceral fat process and present major histocompatibility complex (MHC) class II–restricted antigens. ATMs were sufficient to promote proliferation and interferon-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.
This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db12-1404/-/DC1.
See accompanying commentary, p. 2656.
- Received October 9, 2012.
- Accepted February 28, 2013.
- © 2013 by the American Diabetes Association.
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