Aging is associated with an increase in T cells and inflammatory macrophages in visceral adipose tissue1

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 cell...

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Bibliographic Details
Published in:The Journal of immunology (1950) Vol. 187; no. 12; pp. 6208 - 6216
Main Authors: Lumeng, Carey N., Liu, Jianhua, Geletka, Lynn, Delaney, Colin, DelProposto, Jennifer, Desai, Anjali, Oatmen, Kelsie, Martinez-Santibanez, Gabriel, Julius, Annabelle, Garg, Sanjay, Yung, Raymond L.
Format: Journal Article
Language:English
Published: 09-11-2011
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Summary: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 cell in fat. Therefore, we have performed a detailed examination of ATM subtypes 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 towards a pro-inflammatory 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 PPARγ expression in ATMs and alterations in chemokine/chemokine receptor expression profiles. Furthermore, we have revealed a profound and unexpected expansion of adipose tissue T (ATT) cells in visceral fat with aging that includes a significant induction of regulatory T cells (Tregs) 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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.1102188