A defective CXCL16/CXCR6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblasts
Objective: The maternal–fetal interface undergoes dynamic changes to allow the fetus to grow and develop in the uterus. The interaction between decidual γδ Τ cells and trophoblasts plays a pivotal role during successful pregnancy; however, their physiological functions in early-term human pregnancy...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Wolters Kluwer Health/LWW
2021-01-01
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| Series: | Reproductive and Developmental Medicine |
| Subjects: | |
| Online Access: | http://www.repdevmed.org/article.asp?issn=2096-2924;year=2021;volume=5;issue=3;spage=129;epage=139;aulast=Fan |
| _version_ | 1818117341172465664 |
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| author | Deng-Xuan Fan Ming-Qing Li Wen-Jie Zhou Hong-Lan Huang Hui-Li Yang Cong-Jian Xu |
| author_facet | Deng-Xuan Fan Ming-Qing Li Wen-Jie Zhou Hong-Lan Huang Hui-Li Yang Cong-Jian Xu |
| author_sort | Deng-Xuan Fan |
| collection | DOAJ |
| description | Objective: The maternal–fetal interface undergoes dynamic changes to allow the fetus to grow and develop in the uterus. The interaction between decidual γδ Τ cells and trophoblasts plays a pivotal role during successful pregnancy; however, their physiological functions in early-term human pregnancy are still not completely illustrated. This study was undertaken to illustrate the functional roles of CXCL16/CXCR6 to prevent pregnancy loss via the crosstalk between decidual γδ T cells and HTR8/SVneo trophoblast cells.
Methods: The percentile of CXCR6+ γδ T cells in the peripheral blood from normal female and recurrent spontaneous abortion (RSA) patients was analyzed by flow cytometry. The expression of CXCR6 was detected in decidual immune cells via flow cytometry, and the expression of CXCL16 was analyzed in HTR8/SVneo trophoblast cells and lentivirus (LV)-HTR8/SVneo trophoblast cells via enzyme-linked immunosorbent assay. Reverse transcriptase-polymerase chain reaction was used to verify the expression of the CXCL16 gene in LV-HTR8/SVneo trophoblast cells. Expression of granzyme B and cytokines and proliferation of decidual γδ T cocultured with HTR8/SVneo trophoblast cells were analyzed by flow cytometry. Invasion of HTR8/SVneo trophoblast cells was assessed via Matrigel transwell assay. Adoptive transfer was induced in vivo further to illustrate that the normal expression of CXCL16/CXCR6 could prevent pregnancy loss.
Results: The percentile of CXCR6+ γδ T cells in the peripheral blood from RSA patients was lower than normal pregnancies. The expression of CXCR6 was highest in the decidual γδ T cells among decidual immune cells, and the expression of CXCL16 increased as the amount of HTR8/SVneo trophoblast cells increased. Expression of granzyme B in the decidual γδ T cells was downregulated by cocultured with HTR8/SVneo cells dependent of CXCL16, and HTR8/SVneo trophoblast cells induced the Th2 cytokines production in the decidual γδ T cells. Both the expression of CXCR6 in the decidual γδ T cells and proliferation of the decidual γδ T cells were promoted by HTR8/SVneo trophoblast cells. On the other hand, decidual γδ T cells enhanced the invasion of HTR8/SVneo trophoblast cells and thus promoted embryo implantation. In vivo study was taken further and shown that low expression of CXCL16/CXCR6 results in pregnancy loss because of dialog disorder between decidual γδ Τ cells and trophoblasts.
Conclusions: Low expression of CXCL16/CXCR6 results in pregnancy loss because of the dialog disorder between decidual γδ Τ cells and trophoblasts, and it showed a light on the effective strategy of adoptive transfer of CXCR6+ γδ T cells on the treatment of RSA. This observation provides a scientific basis on which a potential strategy can be applied to the early-detect and treatment of RSA. |
| first_indexed | 2024-12-11T04:36:52Z |
| format | Article |
| id | doaj.art-e7aa68339d954b86a8425785104d07be |
| institution | Directory Open Access Journal |
| issn | 2096-2924 2589-8728 |
| language | English |
| last_indexed | 2024-12-11T04:36:52Z |
| publishDate | 2021-01-01 |
| publisher | Wolters Kluwer Health/LWW |
| record_format | Article |
| series | Reproductive and Developmental Medicine |
| spelling | doaj.art-e7aa68339d954b86a8425785104d07be2022-12-22T01:20:43ZengWolters Kluwer Health/LWWReproductive and Developmental Medicine2096-29242589-87282021-01-015312913910.4103/2096-2924.324878A defective CXCL16/CXCR6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblastsDeng-Xuan FanMing-Qing LiWen-Jie ZhouHong-Lan HuangHui-Li YangCong-Jian XuObjective: The maternal–fetal interface undergoes dynamic changes to allow the fetus to grow and develop in the uterus. The interaction between decidual γδ Τ cells and trophoblasts plays a pivotal role during successful pregnancy; however, their physiological functions in early-term human pregnancy are still not completely illustrated. This study was undertaken to illustrate the functional roles of CXCL16/CXCR6 to prevent pregnancy loss via the crosstalk between decidual γδ T cells and HTR8/SVneo trophoblast cells. Methods: The percentile of CXCR6+ γδ T cells in the peripheral blood from normal female and recurrent spontaneous abortion (RSA) patients was analyzed by flow cytometry. The expression of CXCR6 was detected in decidual immune cells via flow cytometry, and the expression of CXCL16 was analyzed in HTR8/SVneo trophoblast cells and lentivirus (LV)-HTR8/SVneo trophoblast cells via enzyme-linked immunosorbent assay. Reverse transcriptase-polymerase chain reaction was used to verify the expression of the CXCL16 gene in LV-HTR8/SVneo trophoblast cells. Expression of granzyme B and cytokines and proliferation of decidual γδ T cocultured with HTR8/SVneo trophoblast cells were analyzed by flow cytometry. Invasion of HTR8/SVneo trophoblast cells was assessed via Matrigel transwell assay. Adoptive transfer was induced in vivo further to illustrate that the normal expression of CXCL16/CXCR6 could prevent pregnancy loss. Results: The percentile of CXCR6+ γδ T cells in the peripheral blood from RSA patients was lower than normal pregnancies. The expression of CXCR6 was highest in the decidual γδ T cells among decidual immune cells, and the expression of CXCL16 increased as the amount of HTR8/SVneo trophoblast cells increased. Expression of granzyme B in the decidual γδ T cells was downregulated by cocultured with HTR8/SVneo cells dependent of CXCL16, and HTR8/SVneo trophoblast cells induced the Th2 cytokines production in the decidual γδ T cells. Both the expression of CXCR6 in the decidual γδ T cells and proliferation of the decidual γδ T cells were promoted by HTR8/SVneo trophoblast cells. On the other hand, decidual γδ T cells enhanced the invasion of HTR8/SVneo trophoblast cells and thus promoted embryo implantation. In vivo study was taken further and shown that low expression of CXCL16/CXCR6 results in pregnancy loss because of dialog disorder between decidual γδ Τ cells and trophoblasts. Conclusions: Low expression of CXCL16/CXCR6 results in pregnancy loss because of the dialog disorder between decidual γδ Τ cells and trophoblasts, and it showed a light on the effective strategy of adoptive transfer of CXCR6+ γδ T cells on the treatment of RSA. This observation provides a scientific basis on which a potential strategy can be applied to the early-detect and treatment of RSA.http://www.repdevmed.org/article.asp?issn=2096-2924;year=2021;volume=5;issue=3;spage=129;epage=139;aulast=Fancxcl16; cxcr6; decidual γδ t cells; maternal–fetal interface; recurrent spontaneous abortion; trophoblasts |
| spellingShingle | Deng-Xuan Fan Ming-Qing Li Wen-Jie Zhou Hong-Lan Huang Hui-Li Yang Cong-Jian Xu A defective CXCL16/CXCR6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblasts Reproductive and Developmental Medicine cxcl16; cxcr6; decidual γδ t cells; maternal–fetal interface; recurrent spontaneous abortion; trophoblasts |
| title | A defective CXCL16/CXCR6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblasts |
| title_full | A defective CXCL16/CXCR6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblasts |
| title_fullStr | A defective CXCL16/CXCR6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblasts |
| title_full_unstemmed | A defective CXCL16/CXCR6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblasts |
| title_short | A defective CXCL16/CXCR6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblasts |
| title_sort | defective cxcl16 cxcr6 axis increases the risk of pregnancy loss via the abnormal crosstalk between decidual γδ t cells and trophoblasts |
| topic | cxcl16; cxcr6; decidual γδ t cells; maternal–fetal interface; recurrent spontaneous abortion; trophoblasts |
| url | http://www.repdevmed.org/article.asp?issn=2096-2924;year=2021;volume=5;issue=3;spage=129;epage=139;aulast=Fan |
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