CHRU Nancy - Centre Hospitalier Régional Universitaire de Nancy (Siège social : 29 avenue du Maréchal de Lattre de Tassigny, CO 60034, 54035 NANCY CEDEX
Hôpital Central : 29 Avenue du Maréchal de Lattre de Tassigny, 54035 Nancy
Hôpitaux de Brabois / Enfants : Rue du Morvan, 54500 Vandœuvre-lès-Nancy
Maternité régionale :10 Avenue Dr Heydenreich, 54000 Nancy - France)
UB - Université de Bourgogne (Maison de l'université - Esplanade Érasme - BP 27877 - 21078 Dijon cedex - France)
Abstract : Plasmacytoid dendritic cells (pDCs) belong to the family of dendritic cells and possess specific features that distinguish them from conventional dendritic cells. For instance, pDC are the main interferon-alpha-secreting cells. Plasmacytoid dendritic cells exert both proinflammatory and regulatory functions. This is attested by the involvement of pDC through interferon-alpha secretion in several autoimmune diseases, and by the implication of pDC in tolerance. The same is true for TGF-β that plays a dual role in inflammation. In this review, we discuss recent data on pDC and TGF-β interactions. As with many cell types, pDCs are able to respond to TGF-β using the classic Smad signaling pathway. In addition, pDCs are capable to secrete TGF-β, in particular in response to TGF-β exposure. Exposure of pDCs to TGF-β prevents type I interferon secretion in response to TLR7/9 ligands. In contrast, the consequences of TGF-β on the antigen-presenting cell capacities of pDC are less clear, since TGF-β-exposed pDCs may lead to both regulatory T-cell and interleukin-17-secreting cell polarization. Here, we discuss the factors that may influence this polarization. We also discuss how pDCs exposed to TGF-β may participate in tolerance induction and maintenance, or, on the contrary, in autoimmune diseases.
https://www.hal.inserm.fr/inserm-00804423
Contributor : Philippe Saas <>
Submitted on : Monday, March 25, 2013 - 2:55:11 PM Last modification on : Thursday, January 21, 2021 - 2:10:03 PM Long-term archiving on: : Sunday, April 2, 2017 - 8:01:20 PM
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