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Involvement of the JAK ‐ STAT pathway in collagen regulation of decidual NK cells
Author(s) -
Fu Qiang,
Sun Yufei,
Tao Yu,
Piao Hailan,
Wang Xiaoqiu,
Luan Xiying,
Du Meirong,
Li Dajin
Publication year - 2017
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12769
Subject(s) - stat4 , microbiology and biotechnology , small hairpin rna , cytokine , stat , phosphorylation , immunology , biology , cell culture , stat3 , genetics , gene knockdown
Problem The mechanisms underlying the regulation of decidual natural killer cells ( dNK s) at the maternal‐fetal interface are unclear. Method of study Primary trophoblasts ( TRO s), decidual stromal cells ( DSC s), and dNK s were cocultured, and responses to LAIR ‐2 ( LAIR ‐1 inhibitor) and P4H sh RNA (collagen inhibitor) were studied. Results Coculture of dNK s with primary TRO s/ DSC s resulted in downregulation of Th1 cytokine production by dNK s. These effects were abrogated by LAIR ‐2 and P4H sh RNA . LAIR ‐1 binds to SHP ‐1, which in turn binds to JAK 1 and JAK 2. Further, the phosphorylation of STAT 1/ STAT 4 and the expression of the downstream transcription factors T‐bet and Helios in dNK s were decreased by collagen treatment and primary TRO s/ DSC s 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.