Deng-Xuan Fan1, Wen-Jie Zhou1, Li-Ping Jin2, Ming-Qing Li1, Xiang-Hong Xu2, Cong-Jian Xu1,3,4. 1. 1 Obstetrics and Gynecology Hospital, Fudan University, Shanghai, People's Republic of China. 2. 2 Clinical and Translational Research Center, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China. 3. 3 Department of Obstetrics and Gynecology of Shanghai Medical School, Fudan University, Shanghai, People's Republic of China. 4. 4 Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Fudan University, Shanghai, People's Republic of China.
Abstract
BACKGROUND: Decidual γδ T cells are known to regulate the function of trophoblasts at the maternal-fetal interface; however, little is known about the molecular mechanisms of cross talk between trophoblast cells and decidual γδ T cells. METHODS: Expression of chemokine C-X-C motif ligand 6 (CXCL16) and its receptor CXCR6 was evaluated in first-trimester human villus and decidual tissues by immunohistochemistry. γδ T cells were isolated from first-trimester human deciduae and cocultured with JEG3 trophoblast cells. Cell proliferation and apoptosis-related molecules, together with cytotoxicity factor and cytokine production, were measured by flow cytometry analysis. RESULTS: Expression of CXCL16 and CXCR6 was reduced at the maternal-fetal interface in patients who experienced unexplained recurrent spontaneous abortion as compared to healthy pregnancy women. With the administration of pregnancy-related hormones or coculture with JEG3 cells, CXCR6 expression was upregulated on decidual γδ T cells. CXCL16 derived from JEG3 cells caused a decrease in granzyme B production of decidual γδ T cells. In addition, decidual γδ T cells educated by JEG3-derived CXCL16 upregulated the expression of Bcl-xL in JEG3 cells. CONCLUSION: This study suggested that the CXCL16/CXCR6 axis may contribute to maintaining normal pregnancy by reducing the secretion of cytotoxic factor granzyme B of decidual γδ T cells and promoting the expression of antiapoptotic marker Bcl-xL of trophoblasts.
BACKGROUND: Decidual γδ T cells are known to regulate the function of trophoblasts at the maternal-fetal interface; however, little is known about the molecular mechanisms of cross talk between trophoblast cells and decidual γδ T cells. METHODS: Expression of chemokine C-X-C motif ligand 6 (CXCL16) and its receptor CXCR6 was evaluated in first-trimester human villus and decidual tissues by immunohistochemistry. γδ T cells were isolated from first-trimester human deciduae and cocultured with JEG3 trophoblast cells. Cell proliferation and apoptosis-related molecules, together with cytotoxicity factor and cytokine production, were measured by flow cytometry analysis. RESULTS: Expression of CXCL16 and CXCR6 was reduced at the maternal-fetal interface in patients who experienced unexplained recurrent spontaneous abortion as compared to healthy pregnancy women. With the administration of pregnancy-related hormones or coculture with JEG3 cells, CXCR6 expression was upregulated on decidual γδ T cells. CXCL16 derived from JEG3 cells caused a decrease in granzyme B production of decidual γδ T cells. In addition, decidual γδ T cells educated by JEG3-derived CXCL16 upregulated the expression of Bcl-xL in JEG3 cells. CONCLUSION: This study suggested that the CXCL16/CXCR6 axis may contribute to maintaining normal pregnancy by reducing the secretion of cytotoxic factor granzyme B of decidual γδ T cells and promoting the expression of antiapoptotic marker Bcl-xL of trophoblasts.
Authors: Soeren Abel; Christian Hundhausen; Rolf Mentlein; Alexander Schulte; Theo A Berkhout; Neil Broadway; Dieter Hartmann; Radek Sedlacek; Sebastian Dietrich; Barbara Muetze; Bjoern Schuster; Karl-Josef Kallen; Paul Saftig; Stefan Rose-John; Andreas Ludwig Journal: J Immunol Date: 2004-05-15 Impact factor: 5.422
Authors: Manuel Winter; Petra Weissgerber; Karolin Klein; Femke Lux; Daniela Yildiz; Ulrich Wissenbach; Stephan E Philipp; Markus R Meyer; Veit Flockerzi; Claudia Fecher-Trost Journal: Int J Mol Sci Date: 2020-12-18 Impact factor: 5.923