Key result
Diet-induced obesity drives adipose macrophage antigen presentation to promote visceral fat CD4+ T-cell inflammation in mice.
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.
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Morris et al. (2013) studied Dietary obesity and adipose tissue inflammation. Diet-induced obesity vs. Lean state was evaluated on Proliferation of effector memory CD4(+) T cells and interferon-γ production. Diet-induced obesity increased MHC II and costimulatory molecule expression on adipose tissue macrophages, promoting CD4+ T-cell proliferation and interferon-γ production in mice visceral fat.
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