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Review
. 2022 Jul 22:10:826053.
doi: 10.3389/fcell.2022.826053. eCollection 2022.

Regulation and Function of Chemokines at the Maternal-Fetal Interface

Sainan Zhang  1 , Jinli Ding  1 , Yan Zhang  2 , Su Liu  3 , Jing Yang  1 , Tailang Yin  1
Affiliations
Review

Regulation and Function of Chemokines at the Maternal-Fetal Interface

Sainan Zhang et al. Front Cell Dev Biol. .

Abstract

Successful pregnancy requires the maternal immune system to tolerate the semi-allogeneic embryo. A good trophoblast function is also essential for successful embryo implantation and subsequent placental development. Chemokines are initially described in recruiting leukocytes. There are rich chemokines and chemokine receptor system at the maternal-fetal interface. Numerous studies have reported that they not only regulate trophoblast biological behaviors but also participate in the decidual immune response. At the same time, the chemokine system builds an important communication network between fetally derived trophoblast cells and maternally derived decidual cells. However, abnormal functions of chemokines or chemokine receptors are involved in a series of pregnancy complications. As growing evidence points to the roles of chemokines in pregnancy, there is a great need to summarize the available data on this topic. This review aimed to describe the recent research progress on the regulation and function of the main chemokines in pregnancy at the maternal-fetal interface. In addition, we also discussed the potential relationship between chemokines and pregnancy complications.

Keywords: chemokine; chemokine receptor; decidual cells; maternal–fetal interface; pregnancy; trophoblast.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Regulation of main chemokines and chemokine receptors at the maternal–fetal interface. CXCL16 binding to CXCR6 promotes trophoblast invasion and proliferation, as well as endometrium decidualization in an autocrine and paracrine manner, respectively. CXCL16 is also involved in recruiting γδT cells and monocytes. Moreover, CXCL16/CXCR6 can induce M2 phenotype macrophages and decrease their IL-15 levels, which in turn induce the inactivation of NK cells. Trophoblast-derived CXCL12 with CXCR4 not only promotes trophoblast cell migration, invasion, and apoptosis via an autocrine manner but also enhances DSC invasion by upregulating the CXCR4 expression in a paracrine manner. Additionally, the trophoblast-derived CXCL12 also participates in NK cell recruitment and enhances the adhesive abilities of dNK cells to DSCs. CCL2/CCR2 enhances DSC invasion, proliferation, and growth in an autocrine manner. Moreover, CCL2/CCR2 also shows roles in M1/M2 phenotype polarization, monocyte recruitment, Treg recruitment, and Th1/Th2 immune response. CCL3/CCL5/CCR1 plays an essential function in trophoblast invasion.
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