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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >gamma delta T cells promote inflammation and insulin resistance during high fat diet-induced obesity in mice
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gamma delta T cells promote inflammation and insulin resistance during high fat diet-induced obesity in mice

机译：γ-δT细胞在高脂饮食诱导的肥胖症中促进炎症和胰岛素抵抗

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摘要

gamma delta T cells are resident in AT and increase during diet-induced obesity. Their possible contribution to the inflammatory response that accompanies diet-induced obesity was investigated in mice after a 5 to 10 week milk HFD. The HFD resulted in significant increases in CD44(hi), CD62L(lo), and TNF-alpha(+) gamma delta T cells in eAT of WT mice. Mice deficient in all gamma delta T cells (TCR delta(-/-)) or only V gamma 4 and V gamma 6 subsets (V gamma 4/6(-/-)) were compared with WT mice with regard to proinflammatory cytokine production and macrophage accumulation in eAT. Obesity among these mouse strains did not differ, but obese TCR delta(-/-) and V gamma 4/6(-/-) mice had significantly reduced eAT expression of F4/80, a macrophage marker, and inflammatory mediators CCL2 and IL-6 compared with WT mice. Obese TCR delta(-/-) mice had significantly reduced CD11c(+) and TNF-alpha(+) macrophage accumulation in eAT after 5 and 10 weeks on the HFD, and obese V gamma 4/6(-/-) mice had significantly increased CD206(+) macrophages in eAT after 5 weeks on the diet and significantly reduced macrophages after 10 weeks. Obese TCR delta(-/-) mice had significant reductions in systemic insulin resistance and inflammation in liver and skeletal muscle after longer-term HFD feeding (10 and 24 weeks). In vitro studies revealed that isolated gamma delta T cells directly stimulated RAW264.7 macrophage TNF-alpha expression but did not stimulate inflammatory mediator expression in 3T3-L1 adipocytes. These findings are consistent with a role for gamma delta T cells in the proinflammatory response that accompanies diet-induced obesity.
机译：γT细胞驻留在AT中，并在饮食诱导的肥胖过程中增加。在牛奶HFD 5至10周后，研究了它们对饮食引起的肥胖引起的炎症反应的可能贡献。 HFD导致WT小鼠eAT中的CD44（hi），CD62L（lo）和TNF-alpha（+）γ-δT细胞显着增加。将所有γ-δT细胞（TCRδ（-/-））或仅Vγ4和Vγ6子集（Vγ4/6（-/-））缺乏的小鼠与WT小鼠的促炎细胞因子产生进行了比较和巨噬细胞在eAT中的积累。这些小鼠品系之间的肥胖没有差异，但是肥胖的TCR delta（-/-）和V gamma 4/6（-/-）小鼠具有显着降低的F4 / 80，巨噬细胞标志物和炎性介质CCL2和IL的eAT表达。与WT小鼠相比为-6。肥胖的TCR delta（-/-）小鼠在HFD上放置5和10周后，eAT中的CD11c（+）和TNF-α（+）巨噬细胞积累明显减少，肥胖的V gamma 4/6（-/-）小鼠具有饮食5周后eAT中CD206（+）巨噬细胞显着增加，而10周后显着减少巨噬细胞。肥胖的TCR delta（-/-）小鼠在长期HFD喂养（10和24周）后，全身胰岛素抵抗以及肝脏和骨骼肌的炎症显着降低。体外研究表明，分离的γ-δT细胞可直接刺激RAW264.7巨噬细胞TNF-α表达，但不刺激3T3-L1脂肪细胞中的炎症介质表达。这些发现与γ-δT细胞在饮食引起的肥胖症的促炎反应中的作用一致。

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