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|Title:||Intestinal CD103+CD11b− dendritic cells restrain colitis via IFN-γ-induced anti-inflammatory response in epithelial cells||Authors:||Muzaki, Abdul Rashid Bin Mohammad
Loh, S C
Setiagani, Yolanda Aphrilia
|Issue Date:||2015||Source:||Muzaki, A. R. B. M., Tetlak, P., Sheng, J., Loh, S. C., Setiagani, Y. A., Poidinger, M., et al. (2015). Intestinal CD103+CD11b− dendritic cells restrain colitis via IFN-γ-induced anti-inflammatory response in epithelial cells. Mucosal Immunology, 9(2), 336-351.||Series/Report no.:||Mucosal Immunology||Abstract:||A crosstalk between commensals, gut immune cells, and colonic epithelia is required for a proper function of intestinal mucosal barrier. Here we investigated the importance of two distinct intestinal dendritic cell (DC) subsets in controlling intestinal inflammation. We show that Clec9A–diphtheria toxin receptor (DTR) mice after depletion of CD103+CD11b− DCs developed severe, low-dose dextran sodium sulfate (DSS)-induced colitis, whereas the lack of CD103+CD11b+ DCs in Clec4a4-DTR mice did not exacerbate intestinal inflammation. The CD103+CD11b− DC subset has gained a functional specialization that able them to repress inflammation via several epithelial interferon-γ (IFN-γ)-induced proteins. Among others, we identified that epithelial IDO1 and interleukin-18-binding protein (IL-18bp) were strongly modulated by CD103+CD11b− DCs. Through its preferential property to express IL-12 and IL-15, this particular DC subset can induce lymphocytes in colonic lamina propria and in epithelia to secrete IFN-γ that then can trigger a reversible early anti-inflammatory response in intestinal epithelial cells.||URI:||https://hdl.handle.net/10356/81678
|ISSN:||1933-0219||DOI:||10.1038/mi.2015.64||Rights:||This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License. The images or other third partymaterial in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under theCreativeCommons license, userswill need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/||Fulltext Permission:||open||Fulltext Availability:||With Fulltext|
|Appears in Collections:||SBS Journal Articles|
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