Maf deficiency in T cells dysregulates T<sub>reg</sub> - T<sub>H</sub>17 balance leading to spontaneous colitis.

Details

Serval ID
serval:BIB_B94E063539E7
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Maf deficiency in T cells dysregulates T<sub>reg</sub> - T<sub>H</sub>17 balance leading to spontaneous colitis.
Journal
Scientific reports
Author(s)
Imbratta C., Leblond M.M., Bouzourène H., Speiser D.E., Velin D., Verdeil G.
ISSN
2045-2322 (Electronic)
ISSN-L
2045-2322
Publication state
Published
Issued date
16/04/2019
Peer-reviewed
Oui
Volume
9
Number
1
Pages
6135
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
The maintenance of homeostasis in the gut is a major challenge for the immune system. Here we demonstrate that the transcription factor MAF plays a central role in T cells for the prevention of gastro-intestinal inflammation. Conditional knock out mice lacking Maf in all T cells developed spontaneous late-onset colitis, correlating with a decrease of FOXP3 <sup>+</sup> RORγt <sup>+</sup> T cells proportion, dampened IL-10 production in the colon and an increase of inflammatory T <sub>H</sub> 17 cells. Strikingly, FOXP3 <sup>+</sup> specific conditional knock out mice for MAF did not develop colitis and demonstrated normal levels of IL-10 in their colon, despite the incapacity of regulatory T cells lacking MAF to suppress colon inflammation in Rag1 <sup>-/-</sup> mice transferred with naïve CD4 <sup>+</sup> T cells. We showed that one of the cellular sources of IL-10 in the colon of these mice are T <sub>H</sub> 17 cells. Thus, MAF is critically involved in the maintenance of the gut homeostasis by regulating the balance between T <sub>reg</sub> and T <sub>H</sub> 17 cells either at the level of their differentiation or through the modulation of their functions.
Pubmed
Web of science
Open Access
Yes
Create date
28/04/2019 14:23
Last modification date
20/08/2019 15:27
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