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Th17-cell plasticity in Helicobacter hepaticus-induced intestinal inflammation.

Abstract：

:Bacterial-induced intestinal inflammation is crucially dependent on interleukin (IL)-23 and is associated with CD4(+) T helper type 1 (Th1) and Th17 responses. However, the relative contributions of these subsets during the induction and resolution of colitis in T-cell-sufficient hosts remain unknown. We report that Helicobacter hepaticus-induced typhlocolitis in specific pathogen-free IL-10(-/-) mice is associated with elevated frequencies and numbers of large intestinal interferon (IFN)-γ(+) and IFN-γ(+)IL-17A(+) CD4(+) T cells. By assessing histone modifications and transcript levels in IFN-γ(+), IFN-γ(+)IL-17A(+), and IL-17A(+) CD4(+) T cells isolated from the inflamed intestine, we show that Th17 cells are predisposed to upregulate the Th1 program and that they express IL-23R but not IL-12R. Using IL-17A fate-reporter mice, we further demonstrate that H. hepaticus infection gives rise to Th17 cells that extinguish IL-17A secretion and turn on IFN-γ within 10 days post bacterial inoculation. Together, our results suggest that bacterial-induced Th17 cells arising in disease-susceptible hosts contribute to intestinal pathology by switching phenotype, transitioning via an IFN-γ(+)IL-17A(+) stage, to become IFN-γ(+) ex-Th17 cells.

journal_name

Mucosal Immunol

journal_title

Mucosal immunology

authors

Morrison PJ,Bending D,Fouser LA,Wright JF,Stockinger B,Cooke A,Kullberg MC

doi

10.1038/mi.2013.11

subject

Has Abstract

pub_date

2013-11-01 00:00:00

pages

1143-56

issue

6

eissn

1933-0219

issn

1935-3456

pii

mi201311

journal_volume

6

pub_type

杂志文章

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