Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 51, Issue 3, Pages 620-625Publisher
WILEY
DOI: 10.1002/eji.202048714
Keywords
colitis; gut immune system; plasmacytoid dendritic cells; T cells; Clec4C (BDCA2) mice
Categories
Funding
- NovoNordisk Foundation [NNF18OC0033880]
- Paivikki and Sakari Sohlberg Foundation
- Diabetes Research Foundation Finland
- Instrumentarium Research Foundation
- Turku Doctoral Programme of MolecularMedicine (TuDMM), University of Turku
- State research funding for university level health research in Turku University Hospital
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The study revealed an essential role for pDCs in regulating intestinal inflammation during C. rodentium infection, showing their important immune regulatory role in colon-draining lymph nodes.
Dendritic cells (DCs) are first in line to sense invading microbes and to deliver signals to other immune cells. Plasmacytoid DCs (pDC) produce high amounts of type I interferons (IFNs) but also regulate immune responses. Using the Clec4C (BDCA2)-diphtheria toxin receptor mouse model allowing conditional pDC depletion, we identified an essential role for pDCs in regulating intestinal inflammation locally in the gut. In pDC-depleted mice, Citrobacter rodentium infection led to enhanced activation of conventional DCs and induction of IFN-gamma-producing Th1-cells in colon-draining lymph nodes, while induction of Foxp3(+)/CD25(+) Treg and IL-17-producing Th17 cells was impaired. Concomitantly, F4/80(+) macrophages accumulated into the colon lamina propria in excess, and levels of Il-1 beta and Tnf transcripts increased and Foxp3(+) Treg were fewer. Our results indicate that pDCs control inflammation in the gut during C. rodentium infection and that they have an important immune regulatory role in colon-draining lymph nodes.
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