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The CXCL12/CXCR4 axis is involved in the maintenance of Th2 bias at the maternal/fetal interface in early human pregnancy

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Author:
No author available
Journal Title:
Cellular & Molecular Immunology
Issue:
5
DOI:
10.1038/cmi.2012.23
Key Word:
CXCL12/CXCR4;maternal/fetal interface;Th1/Th2

Abstract: The regulatory mechanism of Th2 bias at the maternal/fetal interface remains unclear.In this study,we characterized cytokine production in decidual stromal cells (DSCs),decidual immune cells (DlCs) and embryo-derived trophoblast cells,and investigated the regulation of CXCL12/CXCR4 interaction on Th2 bias at the maternal/fetal interface in early human pregnancy.We found differential production of Th 1-type and Th24-type cytokines by trophoblasts,DSCs and DICs.The secretion of these cytokines varied in different cell cocultures,conduced to Th2 bias.Flow cytometry showed that coculture of trophoblasts with DSCs and DlCs significantly increased IL-4 and IL-10 production in trophoblasts,and IL-10 production in DSCs.However,the coculture of trophoblasts with DSCs and DICs significantly increased interferon (IFN)--γexpression in DSCs,and tumor-necrosis factor (TNF)-α expression in DICs.No change was seen in Th1-type cytokine production in trophoblasts,and in Th2-type cytokine production in DICs in all cocultures.Furthermore,pre-treatment with anti-CXCR4 neutralizing antibody upregulated the production of the Th 1-type cytokines IFN-γ and TNF-α,and downregulated the production of the Th2-type cytokines I L-4 and IL- 10,in trophoblasts,DSCs,DICs or their cocultures.Interestingly,rhCXCL 12 inhibited production of the Th 1-type cytokine TNF-α and enhanced the expression of the Th2-type cytokines such as IL-4,and IL-10 in DICs; this effect was abrogated by anti-CXCR4 antibody.Our present study has elucidated the individual contributions of component cells to the shaping of Th2 bias,and uncovered a complicated cross-talk viathe CXCL 12/CXCR4 signal at the maternal/fetal interface in early human pregnancy.

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