白细胞介素(IL)-2是能够通过激活自然杀伤(NK)细胞来调节免疫应答的关键细胞因子。本研究旨在探讨IL-2激活的NK-92细胞在子宫内膜异位症中的体外治疗潜力。
■分离异位子宫内膜基质细胞(EESCs),并与IL-2激活的NK-92细胞以不同的效应物对靶标(E:T)比率(1:0[对照],1:1、1:3和1:9)。生存能力,细胞毒性,评估IL-2激活的NK-92细胞的细胞表面抗原表达。生存能力,凋亡,入侵,并对不同比例NK-92细胞共培养的EESCs的迁移能力进行评价。凋亡相关蛋白,通过蛋白质印迹检查侵袭和迁移相关蛋白以及MEK/ERK途径。每个实验重复三次。
■IL-2活化以浓度依赖性方式增强NK-92细胞毒性。以1:1、1:3和1:9的E:T比率共培养EESC与IL-2激活的NK-92细胞可将EESC活力降低20%,45%,70%,分别,与对照组相比。EESCs的凋亡率与NK-92细胞比例相关,以1:9的比率观察到最高的比率。此外,IL-2激活的NK-92细胞显著抑制EESC的侵袭和迁移,在1:9的比例下,入侵减少60%,迁移减少50%。此外,在EESCs中,IL-2激活的NK-92细胞下调MEK/ERK信号通路.
IL-2活化的NK-92细胞对EESC表现出有效的细胞毒性作用。它们促进EESC凋亡并抑制活力,入侵,通过调节MEK/ERK信号通路进行迁移。
子宫内膜异位症是一种常见的慢性全身性疾病,影响全球约1.9亿女性。然而,由于缺乏高质量的科学证据和相互矛盾的指南,子宫内膜异位症的临床治疗仍然具有挑战性.本研究旨在探讨白细胞介素(IL)-2是否通过调节子宫内膜基质细胞凋亡和自然杀伤(NK)细胞介导的细胞毒性来影响子宫内膜异位症的进展。从而为子宫内膜异位症提供新的治疗方法。
UNASSIGNED: Interleukin (IL)-2 is a key cytokine capable of modulating the immune response by activating natural killer (NK) cells. This study was recruited to explore the therapeutic potential of IL-2-activated NK-92 cells in endometriosis in vitro.
UNASSIGNED: Ectopic endometrial stromal cells (EESCs) were isolated and co-cultured with IL-2-activated NK-92 cells at varying effector-to-target (E:T) ratios (1:0 [Control], 1:1, 1:3, and 1:9). The viability, cytotoxicity, and cell surface antigen expression of IL-2-activated NK-92 cells were assessed. The viability, apoptosis, invasion, and migration ability of EESCs co-cultured with NK-92 cells at different ratios were evaluated. The apoptosis-related proteins, invasion and migration-related proteins as well as MEK/ERK pathway were examined via western blot. Each experiment was repeated three times.
UNASSIGNED: IL-2 activation enhanced NK-92 cytotoxicity in a concentration-dependent manner. Co-culturing EESCs with IL-2-activated NK-92 cells at E:T ratios of 1:1, 1:3, and 1:9 reduced EESC viability by 20%, 45%, and 70%, respectively, compared to the control group. Apoptosis rates in EESCs increased in correlation with the NK-92 cell proportion, with the highest rate observed at a 1:9 ratio. Moreover, EESC invasion and migration were significantly inhibited by IL-2-activated NK-92 cells, with a 60% reduction in invasion and a 50% decrease in migration at the 1:9 ratio. Besides, the MEK/ERK signalling pathway was down-regulated in EESCs by IL-2-activated NK-92 cells.
UNASSIGNED: IL-2-activated NK-92 cells exhibit potent cytotoxic effects against EESCs. They promote EESC apoptosis and inhibit viability, invasion, and migration through modulating the MEK/ERK signalling pathway.
Endometriosis is a common chronic systemic disease affecting approximately 190 million women worldwide. However, clinical treatments for endometriosis remain challenging due to the scarcity of high-quality scientific evidence and conflicting available guidelines. This research was designed to explore whether interleukin (IL)-2 affected the progression of endometriosis by modulating endometrial stromal cell apoptosis and natural killer (NK) cell-mediated cytotoxicity, thereby providing new therapeutic methods for endometriosis.