Aging Is Associated with an Increase in T Cells and Inflammatory Macrophages in Visceral Adipose Tissue
Author(s) -
Carey N. Lumeng,
Jianhua Liu,
Lynn M. Geletka,
Colin Delaney,
Jennifer L. DelProposto,
Anjali Desai,
Kelsie E. Oatmen,
Gabriel Martinez-Santibañez,
Annabelle Julius,
Sanjay Garg,
Raymond Yung
Publication year - 2011
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1102188
Subject(s) - adipose tissue , adipose tissue macrophages , inflammation , macrophage , inflammatory response , pathology , biology , medicine , microbiology and biotechnology , immunology , endocrinology , white adipose tissue , genetics , in vitro
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 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 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-γ 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.
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