Involvement of the JAK-STAT pathway in collagen regulation of decidual NK cells
Corresponding Author
Qiang Fu
Department of Immunology, Binzhou Medical University, Yantai, China
Correspondence
Qiang Fu, Department of Immunology, Binzhou Medical University, Yantai, China.
Email: [email protected]
and
Dajin Li, Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China.
Email: [email protected]
Search for more papers by this authorYufei Sun
Department of Immunology, Binzhou Medical University, Yantai, China
Search for more papers by this authorYu Tao
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Search for more papers by this authorHailan Piao
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Search for more papers by this authorXiaoqiu Wang
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Search for more papers by this authorXiying Luan
Department of Immunology, Binzhou Medical University, Yantai, China
Search for more papers by this authorMeirong Du
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Search for more papers by this authorCorresponding Author
Dajin Li
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Correspondence
Qiang Fu, Department of Immunology, Binzhou Medical University, Yantai, China.
Email: [email protected]
and
Dajin Li, Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China.
Email: [email protected]
Search for more papers by this authorCorresponding Author
Qiang Fu
Department of Immunology, Binzhou Medical University, Yantai, China
Correspondence
Qiang Fu, Department of Immunology, Binzhou Medical University, Yantai, China.
Email: [email protected]
and
Dajin Li, Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China.
Email: [email protected]
Search for more papers by this authorYufei Sun
Department of Immunology, Binzhou Medical University, Yantai, China
Search for more papers by this authorYu Tao
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Search for more papers by this authorHailan Piao
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Search for more papers by this authorXiaoqiu Wang
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Search for more papers by this authorXiying Luan
Department of Immunology, Binzhou Medical University, Yantai, China
Search for more papers by this authorMeirong Du
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Search for more papers by this authorCorresponding Author
Dajin Li
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China
Correspondence
Qiang Fu, Department of Immunology, Binzhou Medical University, Yantai, China.
Email: [email protected]
and
Dajin Li, Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China.
Email: [email protected]
Search for more papers by this authorAbstract
Problem
The mechanisms underlying the regulation of decidual natural killer cells (dNKs) at the maternal-fetal interface are unclear.
Method of study
Primary trophoblasts (TROs), decidual stromal cells (DSCs), and dNKs were cocultured, and responses to LAIR-2 (LAIR-1 inhibitor) and P4H shRNA (collagen inhibitor) were studied.
Results
Coculture of dNKs with primary TROs/DSCs resulted in downregulation of Th1 cytokine production by dNKs. These effects were abrogated by LAIR-2 and P4H shRNA. LAIR-1 binds to SHP-1, which in turn binds to JAK1 and JAK2. Further, the phosphorylation of STAT1/STAT4 and the expression of the downstream transcription factors T-bet and Helios in dNKs were decreased by collagen treatment and primary TROs/DSCs coculture.
Conclusion
The JAK-STAT pathway and its downstream transcription factors T-bet and Helios are involved in the regulation of dNK function by collagen/LAIR-1 interaction, and this signaling mechanism may contribute to the maintenance of immune tolerance at the maternal-fetal interface.
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