Maf deficiency in T cells dysregulates Treg - TH17 balance leading to spontaneous colitis.

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16 avril 2019

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info:eu-repo/semantics/altIdentifier/doi/10.1038/s41598-019-42486-2

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info:eu-repo/semantics/altIdentifier/pmid/30992496

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info:eu-repo/semantics/altIdentifier/eissn/2045-2322

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_B94E063539E79

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info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/



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C. Imbratta et al., « Maf deficiency in T cells dysregulates Treg - TH17 balance leading to spontaneous colitis. », Serveur académique Lausannois, ID : 10.1038/s41598-019-42486-2


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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 + RORγt + T cells proportion, dampened IL-10 production in the colon and an increase of inflammatory T H 17 cells. Strikingly, FOXP3 + 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 -/- mice transferred with naïve CD4 + T cells. We showed that one of the cellular sources of IL-10 in the colon of these mice are T H 17 cells. Thus, MAF is critically involved in the maintenance of the gut homeostasis by regulating the balance between T reg and T H 17 cells either at the level of their differentiation or through the modulation of their functions.

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