Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters.
Lean, but not obese, fat is enriched for a unique population of regulatory T cells that affect metabolic parameters.
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肥胖伴随着脂肪组织的慢性低度炎症，这会促进胰岛素抵抗和2型糖尿病。脂肪炎症是如何逃脱通常负责防止免疫反应失控的细胞和分子的强大武器装备的？表达转录因子Foxp3的调节性CD4+ T细胞（称为Treg细胞）是一种专门控制免疫反应性的淋巴细胞谱系。具有独特表型的Treg细胞在正常小鼠的腹部脂肪中高度富集，但在肥胖的胰岛素抵抗模型中，该部位的Treg细胞明显减少。在功能丧失和功能获得实验中，Treg细胞调节脂肪组织的炎症状态和胰岛素抵抗。由脂肪驻留调节性T细胞和常规T细胞差异合成的细胞因子直接影响培养的脂肪细胞的炎症介质的合成和葡萄糖摄取。这些发现为利用Treg细胞的抗炎特性来抑制代谢综合征的元素打开了大门。
Obesity is accompanied by chronic, low-grade inflammation of adipose tissue, which promotes insulin resistance and type-2 diabetes. How does fat inflammation escape the powerful armamentarium of cells and molecules normally responsible for guarding against a run-away immune response? Regulatory CD4+ T cells expressing the transcription factor Foxp3 (termed Treg cells) are a lymphocyte lineage specialized in controlling immunologic reactivity. Treg cells with a unique phenotype were highly enriched in the abdominal fat of normal mice, but were strikingly and specifically reduced at this site in insulin-resistant models of obesity. In loss-of-function and gain-of-function experiments, Treg cells regulated the inflammatory state of adipose tissue and insulin resistance. Cytokines differentially synthesized by fat-resident regulatory and conventional T cells directly impacted on the synthesis of inflammatory mediators and glucose uptake by cultured adipocytes. These findings open the door to harnessing the anti-inflammatory properties of Treg cells to inhibit elements of the metabolic syndrome.
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影响因子：
32.4
作者：
Fontenot, JD;Rasmussen, JP;Rudensky, AY
通讯作者：
Rudensky, AY
影响因子：
32.4
作者：
Hill, Jonathan A.;Feuerer, Markus;Benoist, Christophe
通讯作者：
Benoist, Christophe
影响因子：
30.5
作者：
Hsieh, CS;Zheng, Y;Rudensky, AY
通讯作者：
Rudensky, AY
影响因子：
32.4
作者：
Correia-Neves, M;Waltzinger, C;Benoist, C
通讯作者：
Benoist, C
影响因子：
15.3
作者：
Herman, AE;Freeman, GJ;Benoist, C
通讯作者：
Benoist, C