2014年1月7日讯 /生物谷BIOON/ --一项利用小鼠开展的新研究表明，一类不寻常型的免疫细胞即所谓的“γδT细胞”可能是一种新药物靶标，可用于治疗或预防肥胖引起的2型糖尿病。
该研究报告发表在Journal of Leukocyte Biology杂志上，研究表明γδT细胞对于肥胖诱导的巨噬细胞聚集（巨噬细胞聚集与脂肪组织中炎症相关）是必需的。
这种炎症是肥胖引起的，被认为是胰岛素抵抗和2型糖尿病的危险因素，但其根本原因尚未明确。
新的研究结果表明，γδT细胞能导致肥胖小鼠的全身胰岛素抵抗，从而开辟人类肥胖研究的新途径。
在此研究中，科学家用两组小鼠。第一组小鼠改变基因，导致它们缺乏γδT细胞。
第二组小鼠是正常的。当两个组小鼠喂食富含饱和脂肪和糖的西方型饮食，以诱导肥胖，结果发现正常小鼠的脂肪组织，肝和骨骼肌显示较低炎症迹象。
而缺乏γδT细胞小鼠的这些组织炎症反应也降低。此外，与正常小鼠相比，缺乏γδT细胞的肥胖小鼠，全身性胰岛素抵抗减少。
肥胖是一个大型的公共健康健康问题，我们了解肥胖越多，我们就越认识到脂肪组织，炎症和免疫系统之间存在密切联系。（生物谷Bioon.com）
doi:10.1189/jlb.3A0414-211RR
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T cells promote inflammation and insulin resistance during high fat diet-induced obesity in mice.
Pooja Mehta, et al.
γδ 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 CD44hi, CD62Llo, and TNF-α+ γδ T cells in eAT of WT mice. Mice deficient in all γδ T cells (TCRδ-/-) or only Vγ4 and Vγ6 subsets (Vγ4/6-/-) 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 TCRδ-/- and Vγ4/6-/- mice had significantly reduced eAT expression of F4/80, a macrophage marker, and inflammatory mediators CCL2 and IL-6 compared with WT mice. Obese TCRδ?/? mice had significantly reduced CD11c+ and TNF-α+ macrophage accumulation in eAT after 5 and 10 weeks on the HFD, and obese Vγ4/6-/-mice had significantly increased CD206+ macrophages in eAT after 5 weeks on the diet and significantly reduced macrophages after 10 weeks. Obese TCRδ-/- 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 γδ T cells directly stimulated RAW264.7 macrophage TNF-α expression but did not stimulate inflammatory mediator expression in 3T3-L1 adipocytes. These findings are consistent with a role for γδ T cells in the proinflammatory response that accompanies diet-induced obesity.
