The decidual stromal cells-secreted CCL2 induces and maintains decidual leukocytes into Th2 bias in human early pregnancy
Copyright © 2012 Elsevier Inc. All rights reserved.
| Publié dans: | Clinical immunology (Orlando, Fla.). - 1999. - 145(2012), 2 vom: 05. Nov., Seite 161-73 |
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| Auteur principal: | |
| Autres auteurs: | , , , , , |
| Format: | Article en ligne |
| Langue: | English |
| Publié: |
2012
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| Accès à la collection: | Clinical immunology (Orlando, Fla.) |
| Sujets: | Journal Article Research Support, Non-U.S. Gov't Antigens, CD CCL2 protein, human CCR2 protein, human Chemokine CCL2 Culture Media, Conditioned GATA3 Transcription Factor Receptors, CCR2 Recombinant Proteins |
| Résumé: | Copyright © 2012 Elsevier Inc. All rights reserved. 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 |
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| Description: | Date Completed 04.01.2013 Date Revised 02.12.2018 published: Print-Electronic Citation Status MEDLINE |
| ISSN: | 1521-7035 |
| DOI: | 10.1016/j.clim.2012.07.017 |