Department of Medical Biochemistry, Molecular Biology and Immunology, University of Seville Medical School, Seville, Spain.
CABIMER-Andalusian Center for Molecular Biology and Regenerative Medicine (CSIC-University of Seville-UPO-Junta de Andalucia), Seville, Spain.
Obes Surg. 2018 Sep;28(9):2774-2782. doi: 10.1007/s11695-018-3215-y.
The immune response of visceral adipose tissue (VAT) in obesity, in particular the role of invariant natural killer T (iNKT) cells, has not yet been fully elucidated.
To characterize iNKT cells and its activation status in VAT and peripheral blood mononuclear cells (PBMC) in morbidly obese subjects (MO), and to analyze their association with metabolic parameters.
Twenty non-obese and 20 MO subjects underwent Roux-en-Y gastric bypass (RYGB) and were studied before and 6 months after RYGB. VAT and PBMC were obtained.
A decrease in VAT iNKT cells from MO was found, however, not in PBMC. Visceral adipocytes from MO presented increased CD1d expression (p = 0.032). MO presented an increase in early activated CD69+ iNKT cells in PBMC before RYGB (p < 0.001), but not after RYGB nor in VAT, and an increase in later activated CD25+ iNKT in VAT (p = 0.046), without differences in PBMC. The co-expression of early and later markers (CD69+CD25+) in iNKT cells was increased in MO in VAT (p = 0.050) and PBMC (p = 0.006), decreasing after RYGB (p = 0.050). CD69+ iNKT and CD69+CD25+ iNKT cells in PBMC after RYGB correlated negatively with glucose, insulin, and insulin resistance levels.
There is a tissue-specific phenotype and activation of iNKT cells in VAT in morbid obesity, which could be involved in VAT immunometabolism dysregulation. Also, the increase in CD1d expression could be to offset the lack of VAT iNKT cells.
肥胖患者内脏脂肪组织（VAT）的免疫反应，特别是不变自然杀伤 T（iNKT）细胞的作用，尚未完全阐明。
描述病态肥胖（MO）患者 VAT 和外周血单个核细胞（PBMC）中 iNKT 细胞及其激活状态，并分析其与代谢参数的相关性。
20 名非肥胖者和 20 名 MO 患者接受 Roux-en-Y 胃旁路手术（RYGB），分别在 RYGB 术前和术后 6 个月进行研究。获取 VAT 和 PBMC。
MO 患者 VAT 中的 iNKT 细胞减少，但 PBMC 中没有。MO 患者的内脏脂肪细胞 CD1d 表达增加（p = 0.032）。MO 患者在 RYGB 术前 PBMC 中早期激活的 CD69+iNKT 细胞增加（p < 0.001），但 RYGB 后和 VAT 中没有增加，VAT 中晚期激活的 CD25+iNKT 细胞增加（p = 0.046），而 PBMC 中没有差异。VAT 和 PBMC 中 iNKT 细胞的早期和晚期标志物（CD69+CD25+）的共表达在 MO 中增加（p = 0.050），RYGB 后减少（p = 0.050）。RYGB 后 PBMC 中的 CD69+iNKT 和 CD69+CD25+iNKT 细胞与血糖、胰岛素和胰岛素抵抗水平呈负相关。
在病态肥胖的 VAT 中存在组织特异性 iNKT 细胞表型和激活，这可能与 VAT 免疫代谢失调有关。此外，CD1d 表达的增加可能是为了弥补 VAT iNKT 细胞的缺乏。
