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National Institute of Environmental Health Sciences

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Publication Detail

Title: Changes in adipose tissue macrophages and T cells during aging.

Authors: Garg, Sanjay K; Delaney, Colin; Shi, Hang; Yung, Raymond

Published In Crit Rev Immunol, (2014)

Abstract: Adipose tissue historically was believed to be an inert tissue, functioning primarily in the storage of energy and thermal homeostasis. However, recent discoveries point toward a critical role for adipocytes in endocrine function as well as immune regulation. Excess body fat, accumulated through aging and/or a calorie-rich diet, is associated with many chronic metabolic and inflammatory diseases. Within the stromal vascular fraction of adipose tissue, macrophages and T cells accumulate with increasing tissue mass, secreting pro- or anti-inflammatory cytokines. In this review we discuss the current understanding of immune cell function in both diet-induced and age-related obesity. In both models of obesity, the classically activated, pro-inflammatory (M1) subtype takes precedence over the alternatively activated, anti-inflammatory (M2) macrophages, causing tissue necrosis and releasing pro-inflammatory cytokines like interleukin-6. Other distinct adipose tissue macrophage subtypes have been identified by surface marker expression and their functions characterized. Adipose tissue T cell recruitment to adipose tissue is also different between aging- and diet-induced obesity. Under both conditions, T cells exhibit restricted T-cell receptor diversity and produce higher levels of pro-inflammatory signals like interferon-γ and granzyme B relative to young or healthy mice. However, numbers of regulatory T cells are dramatically different between the 2 models of obesity. Taken together, these findings suggest models of age- and diet-induced obesity may be more distinct than previously thought, with many questions yet to be resolved in this multidimensional disease.

PubMed ID: 24579699 Exiting the NIEHS site

MeSH Terms: Adipose Tissue/immunology*; Aging/immunology*; Animals; Cytokines/metabolism; Humans; Inflammation Mediators/metabolism; Macrophages/immunology*; Mice; Obesity/immunology*; T-Lymphocytes/immunology*

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