4.6 Article

Aging Is Associated with an Increase in T Cells and Inflammatory Macrophages in Visceral Adipose Tissue

Journal

JOURNAL OF IMMUNOLOGY
Volume 187, Issue 12, Pages 6208-6216

Publisher

AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1102188

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Funding

  1. National Institutes of Health [RO1AG020628, RO1AG028268, RO1AR042525, R01DK090262, K08DK078851]
  2. Veterans Affairs Merit Review grant
  3. Ann Arbor Department of Veterans Affairs Geriatric Research Education and Clinical Centers
  4. University of Michigan Claude D. Pepper Older Americans Independence Center National Institute on Aging [P30AG024824]
  5. Nathan Shock Center National Institute on Aging [AG013283]
  6. Core Center National Institute of Environmental Health Sciences [UM-P30, P30ES017885]

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Age-related adiposity has been linked to chronic inflammatory diseases in late life. To date, the studies on adipose tissue leukocytes and aging have not taken into account the heterogeneity of adipose tissue macrophages (ATMs), nor have they examined how age impacts other leukocytes such as T cells in fat. Therefore, we have performed a detailed examination of ATMsubtypes in young and old mice using state of the art techniques. Our results demonstrate qualitative changes in ATMs with aging that generate a decrease in resident type 2 (M2) ATMs. The profile of ATMs in old fat shifts toward a proinflammatory environment with increased numbers of CD206(-)CD11c(-) (double-negative) ATMs. The mechanism of this aging-induced shift in the phenotypic profile of ATMs was found to be related to a decrease in peroxisome proliferator-activated receptor-gamma expression in ATMs and alterations in chemokine/chemokine receptor expression profiles. Furthermore, we have revealed a profound and unexpected expansion of adipose tissue T cells in visceral fat with aging that includes a significant induction of regulatory T cells in fat. Our findings demonstrate a unique inflammatory cell signature in the physiologic context of aging adipose tissue that differs from those induced in setting of diet-induced obesity. The Journal of Immunology, 2011, 187: 6208-6216.

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