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Critical Reviews™ in Immunology
インパクトファクター: 1.404 5年インパクトファクター: 3.347 SJR: 0.706 SNIP: 0.55 CiteScore™: 2.19

ISSN 印刷: 1040-8401
ISSN オンライン: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.2013005868
pages 529-553

Functions of TGF-β-Exposed Plasmacytoid Dendritic Cells

Philippe Saas
INSERM UMR1098, F25020 Besancon cedex, France; Universite de Franche-Comte, SFR FED4234, F25000 Besancon cedex, France; EFS Bourgogne Franche-Comte, F25020 Besancon cedex, France; LabEX LipSTIC, ANR-11-LABX-0021, F25020 Besancon cedex, France
Sylvain Perruche
INSERM UMR1098, F25020 Besancon cedex, France; Universite de Franche-Comte, SFR FED4234, F25000 Besancon cedex, France; EFS Bourgogne Franche-Comte, F25020 Besancon cedex, France; LabEX LipSTIC, ANR-11-LABX-0021, F25020 Besancon cedex, France

要約

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.


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