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周围血液iNKT细胞表现出激活的形状,既增加了细胞亡,也导致肥胖症的功能障碍

Chloé Wilkin¹, Nathalie Esser^1,2, Cédric Lassence³

¹Laboratory of Immunometabolism and Nutrition, GIGA-Immunobiology, ULiège, Liège, Belgium.

Frontiers in immunology

|September 26, 2025

概括

肥胖会通过激活不变天然杀手T (iNKT) 细胞和对单细胞的CD1d进行上调来损害免疫功能. 减肥手术逆转了这些与肥胖相关的免疫变化,这表明CD1d和iNKT细胞功能障碍之间存在联系.

科学领域:

免疫学免疫学免疫学
代谢障碍代谢障碍代谢障碍
细胞生物学细胞生物学

背景情况:

肥胖与慢性炎症和免疫细胞功能障碍有关.
不变的自然杀手T (iNKT) 细胞是通过CD1d识别脂质抗原的关键免疫细胞.
功能失调的iNKT细胞可能导致肥胖症免疫监测受损.

研究的目的:

研究肥胖或不肥胖个体中iNKT细胞的激活,亡和功能.
为了检查CD1d在肥胖症单细胞上的表达及其与iNKT细胞状态的相关性.
评估减肥手术对iNKT细胞和肥胖症中CD1d表达的影响.

主要方法:

来自肥胖或不肥胖个体的外周血液iNKT细胞的分析.
评估iNKT细胞激活,细胞亡和对刺激的反应.
流细胞计,以评估单细胞子集上的CD1d表达.
减肥手术前后免疫参数的比较.

主要成果:

在肥胖个体中,iNKT细胞的激活和亡增加,特别是CD4子集.
肥胖与中等和非经典单细胞上调的CD1d相关,与iNKT细胞功能障碍相关.
腹腔外科手术显著逆转了iNKT细胞激活,低反应性和单细胞CD1d调节.

结论:

肥胖诱导iNKT细胞激活和功能障碍,可能通过单细胞上增加的CD1d表达来调解.
上调的CD1d可能会增强脂质抗原的呈现,有助于肥胖症中iNKT细胞的激活.
腹腔外科手术通过逆转iNKT细胞和CD1d变化,显示出恢复肥胖患者免疫平衡的潜力.

关键词:

CD1d 是一个CD1d.激活标记器的激活标记器细胞因子细胞因子 iNKTT 在线观看在线观看脂质抗原是一种抗原.单细胞 (Monocytes) 是一种单细胞.肥胖肥胖肥胖肥胖肥胖肥胖肥胖肥胖

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