Human fetal dendritic cells promote prenatal T-cell immune suppression through arginase-2

Naomi McGovern, Amanda Shin, Gillian Low, Donovan Low, Kaibo Duan, Leong Jing Yao, Rasha Msallam, Ivy Low, Nurhidaya Binte Shadan, Hermi R. Sumatoh, Erin Soon, Josephine Lum, Esther Mok, Sandra Hubert, Peter See, Edwin Huang Kunxiang, Yie Hou Lee, Baptiste Janela, Mahesh Choolani, Citra Nurfarah Zaini MattarYiping Fan, Tony Kiat Hon Lim, Dedrick Kok Hong Chan, Ker Kan Tan, John Kit Chung Tam, Christopher Schuster, Adelheid Elbe-Bürger, Xiao Nong Wang, Venetia Bigley, Matthew Collin, Muzlifah Haniffa, Andreas Schlitzer, Michael Poidinger, Salvatore Albani, Anis Larbi, Evan W. Newell, Jerry Kok Yen Chan, Florent Ginhoux

Résultats de recherche: Contribution à un journalArticleRevue par des pairs

196 Citations (Scopus)

Résumé

During gestation the developing human fetus is exposed to a diverse range of potentially immune-stimulatory molecules including semi-allogeneic antigens from maternal cells, substances from ingested amniotic fluid, food antigens, and microbes. Yet the capacity of the fetal immune system, including antigen-presenting cells, to detect and respond to such stimuli remains unclear. In particular, dendritic cells, which are crucial for effective immunity and tolerance, remain poorly characterized in the developing fetus. Here we show that subsets of antigen-presenting cells can be identified in fetal tissues and are related to adult populations of antigen-presenting cells. Similar to adult dendritic cells, fetal dendritic cells migrate to lymph nodes and respond to toll-like receptor ligation; however, they differ markedly in their response to allogeneic antigens, strongly promoting regulatory T-cell induction and inhibiting T-cell tumour-necrosis factor-α production through arginase-2 activity. Our results reveal a previously unappreciated role of dendritic cells within the developing fetus and indicate that they mediate homeostatic immune-suppressive responses during gestation.

langue originaleAnglais
Pages (de - à)662-666
Nombre de pages5
journalNature
Volume546
Numéro de publication7660
Les DOIs
étatPublié - 29 juin 2017
Modification externeOui

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