Abstract
Chronic inflammation in adipose tissue, possibly related to adipose cell hypertrophy, hypoxia, and/or intestinal leakage of bacteria and their metabolic products, likely plays a critical role in the development of obesity-associated insulin resistance (IR). Cells of both the innate and adaptive immune system residing in adipose tissues, as well as in the intestine, participate in this process. Thus, M1 macrophages, IFN-γ-secreting Th1 cells, CD8+ T cells, and B cells promote IR, in part through secretion of proinflammatory cytokines. Conversely, eosinophils, Th2 T cells, type 2 innate lymphoid cells, and possibly Foxp3+ Tregs protect against IR through local control of inflammation.
Publication types
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Review
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adaptive Immunity*
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Adipose Tissue / immunology*
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Adipose Tissue / pathology
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Animals
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B-Lymphocytes / immunology
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B-Lymphocytes / pathology
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CD8-Positive T-Lymphocytes / immunology
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CD8-Positive T-Lymphocytes / pathology
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Eosinophils / immunology
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Eosinophils / pathology
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Humans
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Immunity, Innate*
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Insulin Resistance / immunology*
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Interferon-gamma / immunology
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Intestines / immunology
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Intestines / pathology
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Macrophages / immunology
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Macrophages / pathology
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Obesity / complications
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Obesity / immunology*
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Obesity / pathology
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T-Lymphocytes, Regulatory / immunology
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T-Lymphocytes, Regulatory / pathology
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Th2 Cells / immunology
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Th2 Cells / pathology
Substances
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IFNG protein, human
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Interferon-gamma