- Poster presentation
- Open Access
Altered innate functions of myeloid dendritic cells in ANCA-associated vasculitis
© Braudeau et al; licensee BioMed Central Ltd. 2012
- Published: 28 November 2012
- Dendritic Cell
- Intracellular Cytokine
- Plasmacytoid Dendritic Cell
- Altered Response
- Critical Effector
Dendritic cells (DC) are critical effectors of innate and adaptive immunity, acting both as sentinels that detect the presence of pathogens and as key antigen-presenting cells that regulate the adaptive immune response. Therefore, DC play a crucial role in the control of autoimmune responses. We previously showed that blood DC numbers were strongly reduced in ANCA-associated vasculitis (AAV) likely due to their recruitment in tissues. Here, we assessed the ex vivo responsiveness of blood DC from AAV-patients to Toll-like receptors (TLRs) stimulation.
Blood samples from 10 untreated patients with AAV during flares and before any immunosuppressive treatment (AP) were analyzed, along with 9 AAV patients in remission (RP) and 11 age-matched healthy controls (HC). Intracellular cytokine (IL-12, TNF-α, IFN-α) production by blood DC was assessed by 8-colors flow cytometry after stimulation by Toll-like receptors of whole blood samples.
We found that myeloid DC (mDC) from patients in acute phase exhibited a decreased IL-12 production after TLR3, 4 and 7/8 stimulation compared to patients in remission and healthy controls. These mDC also produced less TNF-α after TLR3 stimulation. Moreover, we observed a reduction in the frequency TNFα-producing plasmacytoid DC (pDC) upon TLR7/8 triggering in AP patients compared to RP patients and HC.
Our data show that circulating mDC from patients with AAV exhibited an altered response to several TLR ligands, with a notable decrease in IL-12 production. These unexpected results suggest the innate functions of DC especially in response to pathogens are impaired during AAV.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.