In obesity, adipose tissue undergoes dynamic remodeling processes such as adipocyte hypertrophy, hypoxia, immune responses, and adipocyte death. However, whether and how invariant natural killer T (iNKT) cells contribute to adipose tissue remodeling are elusive. In this study, we demonstrate that iNKT cells remove unhealthy adipocytes and stimulate the differentiation of healthy adipocytes. In obese adipose tissue, iNKT cells were abundantly found nearby dead adipocytes. FasL-positive adipose iNKT cells exerted cytotoxic effects to eliminate hypertrophic and pro-inflammatory Fas-positive adipocytes. Furthermore, in vivo adipocyte-lineage tracing mice model showed that activation of iNKT cells by alpha-galactosylceramide promoted adipocyte turnover, eventually leading to potentiation of the insulin-dependent glucose uptake ability in adipose tissue. Collectively, our data propose a novel role of adipose iNKT cells in the regulation of adipocyte turnover in obesity.

中文翻译：

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不变的自然杀伤性T细胞的激活通过脂肪细胞的死亡和肥胖引起的出生来刺激脂肪组织的重塑。

在肥胖症中，脂肪组织会经历动态重塑过程，例如脂肪细胞肥大，缺氧，免疫反应和脂肪细胞死亡。然而，是否恒定的自然杀伤T细胞（iNKT）是否有助于脂肪组织重塑尚不清楚。在这项研究中，我们证明了iNKT细胞去除了不健康的脂肪细胞并刺激了健康脂肪细胞的分化。在肥胖的脂肪组织中，大量的iNKT细胞被发现在附近的死亡脂肪细胞中。FasL阳性脂肪iNKT细胞发挥细胞毒作用，以消除肥大性和促炎性Fas阳性脂肪细胞。此外，体内脂肪细胞谱系追踪小鼠模型显示，α-半乳糖基神经酰胺对iNKT细胞的激活促进了脂肪细胞的更新，最终导致了脂肪组织中胰岛素依赖性葡萄糖摄取能力的增强。