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Critical Reviews™ in Immunology
インパクトファクター: 1.352 5年インパクトファクター: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN 印刷: 1040-8401
ISSN オンライン: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.2013006833
pages 1-14

Changes in Adipose Tissue Macrophages and T Cells During Aging

Sanjay K. Garg
Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan
Colin Delaney
Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan
Hang Shi
Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan
Raymond Yung
Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan

要約

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.


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