title: Changes in adipose tissue macrophages and T cells during aging.
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.
authors.affiliation: Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan.
authors.forename: Sanjay K
authors.initials: SK
authors.lastname: Garg
authors.affiliation: Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan.
authors.forename: Colin
authors.initials: C
authors.lastname: Delaney
authors.affiliation: Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan.
authors.forename: Hang
authors.initials: H
authors.lastname: Shi
authors.affiliation: Department of Internal Medicine, University of Michigan School of Medicine, Ann Arbor, Michigan.
authors.forename: Raymond
authors.initials: R
authors.lastname: Yung
mesh_terms: D000273:Adipose Tissue / Q000276:immunology*; D000375:Aging / Q000276:immunology*; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008264:Macrophages / Q000276:immunology*; D051379:Mice; D009765:Obesity / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators