Format

Send to

Choose Destination
Mucosal Immunol. 2017 May;10(3):695-704. doi: 10.1038/mi.2016.87. Epub 2016 Oct 12.

The regulatory dendritic cell marker C1q is a potent inhibitor of allergic inflammation.

Author information

1
Research Department, Stallergenes Greer, Antony, France.
2
CEA, Fontenay-aux-roses, France.
3
CNRS UMR7211 & INSERM U959, Hôpital Pitié-Salpêtrière, Paris, France.
4
Artimmune SAS, Orléans, France.
5
CNRS UMR 7355-University of Orléans, Orléans, France.

Abstract

The complement subunit C1q was recently identified as a marker for monocyte-derived regulatory dendritic cells supporting the differentiation of interleukin (IL)-10-secreting CD4+ T cells with a suppressive activity. Furthermore, C1q expression is upregulated in peripheral blood mononuclear cells of allergic patients in the course of successful allergen immunotherapy. Herein, we investigated a potential direct role of C1q in downregulating allergic inflammation. In mice with ovalbumin (OVA) or birch pollen (BP)-induced allergic asthma, C1q is as efficacious as dexamethasone to reduce both airway hyperresponsiveness (AHR), eosinophil, and ILC2 infiltrates in bronchoalveolar lavages, as well as allergen-specific T helper 2 cells in the lungs. Administration of C1q does not expand IL-10+/Foxp3+ regulatory T cells in the lungs, spleen, or in the blood. Depletion of plasmacytoid dendritic cells (pDCs) abrogates the capacity of C1q to reduce AHR and eosinophilic infiltrates in OVA-sensitized mice. Also C1q treatment inhibits the activation of human and mouse pDCs by CpGs, thereby demonstrating a critical role for pDCs in the anti-inflammatory activity of C1q. We conclude that regulatory dendritic cells can mediate a potent direct anti-inflammatory activity via the expression and/or secretion of molecules such as C1q, independently of their capacity to expand the pool of regulatory T cells.

PMID:
27731323
DOI:
10.1038/mi.2016.87
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center