Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3257131 | Clinical Immunology | 2012 | 13 Pages |
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.