Fat Treg cells: a liaison between the immune and metabolic systems

By M. Feuerer, Laura Herrero, D. Cipolletta, A. Naaz, Jamie Wong, A. Nayer, Jongsoon Lee, A. Goldfine, C. Benoist, S. Shoelson and 1 more. Nature Medicine, 2009

2,038 citations recorded by the source corpus.

Obesity is accompanied by chronic, low-grade inflammation of adipose tissue, which promotes insulin resistance and type-2 diabetes. These findings raise the question of how fat inflammation can escape the powerful armamentarium of cells and molecules normally responsible for guarding against a runaway immune response. CD4+ Foxp3+ T regulatory (Treg) cells with a unique phenotype were highly enriched in the abdominal fat of normal mice, but their numbers were strikingly and specifically reduced at this site in insulin-resistant models of obesity. Loss-of-function and gain-of-function experiments revealed that these Treg cells influenced the inflammatory state of adipose tissue and, thus, insulin resistance. Cytokines differentially synthesized by fat-resident regulatory and conventional T cells directly affected the synthesis of inflammatory mediators and glucose uptake by cultured adipocytes. These observations suggest that harnessing the anti-inflammatory properties of Treg cells to inhibit elements of the metabolic syndrome may have therapeutic potential.

Subfields: Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/ba50d2e03d4fd25c66f7706834f56b7390303e52

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Citations in the corpus

Inflammation as a link between obesity, metabolic syndrome and type 2 diabetes. (2014, background): “The regulatory T lymphocytes express high amount of the anti-inflammatory cytokine IL-10 which inhibit macrophage migration and induce the differentiation of M2 macrophages [35,37].”
Impact of Obesity and Metabolic Syndrome on Immunity. (2016, background): “The reduction in certain lymphocyte subsets may coincide with concomitant increases in T cells that respond to antigens unique to dysfunctional adipose and lymphocytes that favor metabolic tissue infiltration and proinflammatory responses (13, 20).”
Endoplasmic Reticulum Stress and the Inflammatory Basis of Metabolic Disease (2010, neutral): “In particular, chronic inflammation of adipose tissue (and recruitment of professional immune cells to this site) (Alexaki et al., 2009; Feuerer et al., 2009; Liu et al., 2009; Nishimura et al., 2009; Winer et al., 2009), whether triggered metabolically or through injury or death of adipocytes, can ”
Adipose Tissue Remodeling: Its Role in Energy Metabolism and Metabolic Disorders (2016, background): “In Treg cell-deficient mice, HFD-induced insulin resistance and expression of pro-inflammatory cytokines in the adipose tissue are exacerbated (155).”
Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages (2013, background): “Finally, IL5– and IL13–expressing Th2 cells accumulate in VAT of older animals on normal diet (ND; unpublished data), and similar to VAT T reg cells (Feuerer et al., 2009), may provide an additional layer of adaptive regulation to maintain metabolic homeostasis.”
Human T cell development, localization, and function throughout life (2018, background): “Treg cells have also been identified in human fat with decreased Treg cells correlating with obesity (Feuerer et al., 2009).”