4.7 Article

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

Journal

DIABETES
Volume 62, Issue 8, Pages 2762-2772

Publisher

AMER DIABETES ASSOC
DOI: 10.2337/db12-1404

Keywords

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Funding

  1. National Institutes of Health (NIH) [DK-090262, DK-078851, DK-087999, DK-092873, T32-HD-008513, DK-089503]
  2. NIH National Research Service Award [DK-091976]
  3. NIH Cellular and Molecular Biology Training Grant [T32-GM-007315]
  4. Pediatric Endocrine Society Research Fellowship Award
  5. Chemistry Core(s) at the Michigan Diabetes Research and Training Center
  6. National Institute of Diabetes and Digestive and Kidney Diseases [P60-DK-020572]

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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-gamma-producing CD4(+) T cells in adipose tissue. ATMs from lean and obese visceral fat process and present major histocompatibility complex (NBC) class II-restricted antigens. ATMs were sufficient to promote proliferation and interferon-gamma production from antigen-specific CD4(+) T cells in vitro and in vivo. Diet-induced obesity increased the expression of AMC 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. Diabetes 62:2762-2772, 2013

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