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Am J Reprod Immunol. 2017 Dec;78(6). doi: 10.1111/aji.12769. Epub 2017 Oct 4.

Involvement of the JAK-STAT pathway in collagen regulation of decidual NK cells.

Author information

1
Department of Immunology, Binzhou Medical University, Yantai, China.
2
Hospital and Institute of Obstetrics & Gynecology, Fudan University, Shanghai, China.

Abstract

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.

KEYWORDS:

JAK-STAT; LAIR-1; collagen; decidual NK cells

PMID:
28975683
DOI:
10.1111/aji.12769
[Indexed for MEDLINE]

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