NK-92 cells activated by IL-2 inhibit the progression of endometriosis in vitro

Background 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.Methods Ectopic endometrial stromal cells (EESCs) w...

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Main Authors: Jun Yao, Li-jiao Zhang, Zhe Zhou, Mao-fang Hua
Format: Article
Language:English
Published: Taylor & Francis Group 2024-12-01
Series:Journal of Obstetrics and Gynaecology
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Online Access:https://www.tandfonline.com/doi/10.1080/01443615.2024.2372682
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author Jun Yao
Li-jiao Zhang
Zhe Zhou
Mao-fang Hua
author_facet Jun Yao
Li-jiao Zhang
Zhe Zhou
Mao-fang Hua
author_sort Jun Yao
collection DOAJ
description Background 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.Methods 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.Results 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.Conclusion 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.
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series Journal of Obstetrics and Gynaecology
spelling doaj-art-e76f7f859e7e4f288096a94787673ab12025-01-09T12:13:17ZengTaylor & Francis GroupJournal of Obstetrics and Gynaecology0144-36151364-68932024-12-0144110.1080/01443615.2024.2372682NK-92 cells activated by IL-2 inhibit the progression of endometriosis in vitroJun Yao0Li-jiao Zhang1Zhe Zhou2Mao-fang Hua3Department of Gynecology, Lianyungang Maternal and Child Health Hospital, Lianyungang, Jiangsu, ChinaDepartment of Obstetrics, Lianyungang Maternal and Child Health Hospital, Lianyungang, Jiangsu, ChinaDepartment of Gynecology, Lianyungang Maternal and Child Health Hospital, Lianyungang, Jiangsu, ChinaDepartment of Gynecology, Lianyungang Maternal and Child Health Hospital, Lianyungang, Jiangsu, ChinaBackground 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.Methods 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.Results 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.Conclusion 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.https://www.tandfonline.com/doi/10.1080/01443615.2024.2372682Endometriosisectopic endometrial stromal cellsNK-92 cellsIL-2MEK/ERK signalling pathway
spellingShingle Jun Yao
Li-jiao Zhang
Zhe Zhou
Mao-fang Hua
NK-92 cells activated by IL-2 inhibit the progression of endometriosis in vitro
Journal of Obstetrics and Gynaecology
Endometriosis
ectopic endometrial stromal cells
NK-92 cells
IL-2
MEK/ERK signalling pathway
title NK-92 cells activated by IL-2 inhibit the progression of endometriosis in vitro
title_full NK-92 cells activated by IL-2 inhibit the progression of endometriosis in vitro
title_fullStr NK-92 cells activated by IL-2 inhibit the progression of endometriosis in vitro
title_full_unstemmed NK-92 cells activated by IL-2 inhibit the progression of endometriosis in vitro
title_short NK-92 cells activated by IL-2 inhibit the progression of endometriosis in vitro
title_sort nk 92 cells activated by il 2 inhibit the progression of endometriosis in vitro
topic Endometriosis
ectopic endometrial stromal cells
NK-92 cells
IL-2
MEK/ERK signalling pathway
url https://www.tandfonline.com/doi/10.1080/01443615.2024.2372682
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AT maofanghua nk92cellsactivatedbyil2inhibittheprogressionofendometriosisinvitro