The decidual stromal cells-secreted CCL2 induces and maintains decidual leukocytes into Th2 bias in human early pregnancy

The precise mechanism of characteristic Th2 predominance at maternal–fetal interface remains unresolved. In the present study, we investigated roles of the decidua-derived CCL2 in Th2 predominance at maternal–fetal interface. FCM shows that 55% CD56+CD16−CD3− decidual NK, 52% CD4+ T cells and 75% CD14+ monocytes express CCR2. Recombinant human CCL2 (rhCCL2) and the decidual stromal cells (DSCs)-derived supernatant can enhance proliferation and inhibit apoptosis of these decidual leukocytes (DLCs), and promote Th2 cytokines production, IL-4 and IL-10, with an increase in GATA-3 transcription. They also inhibit the secretion of Th1 cytokines, TNF-α and IFN-γ, with a decrease in T-bet transcription It is concluded that the secreted CCL2 by decidual stromal cells increases GATA-3 transcription and decreases T-bet transcription in the decidual leukocytes, which contributes to Th2 polarization at maternal–fetal interface. Furthermore, the Th2 cytokines, IL-4 and IL-10, rather than Th1 cytokines, was shown to increase CCL2 secretion of DSC.

► DSCs-secreted CCL2 increases GATA-3 and decreases T-bet in decidual leukocytes.
► Th2 cytokines, IL-4 and IL-10, increase CCL2 secretion of DSC.
► The DSCs-derived CCL2 is in favor of Th2 bias in successful pregnancy.