T-bet-independent Th1 response induces intestinal immunopathology during Toxoplasma gondii infection.

T-bet-independent Th1 response induces intestinal immunopathology during Toxoplasma gondii infection.
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DOI:
10.1038/mi.2017.102
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发表时间:
2018-05
期刊:
影响因子:
8
通讯作者:
Yarovinsky F
Yarovinsky F
中科院分区:
医学1区
文献类型:
--
作者:
López-Yglesias AH;Burger E;Araujo A;Martin AT;Yarovinsky F

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Coordinated production of IFN-γ by innate and adaptive immune cells is central for host defense, but can also trigger immunopathology. The investigation of the lymphoid cell-specific contribution to the IFN-γ-mediated intestinal pathology during Toxoplasma gondii infection identified CD4+ T cells as a key cell population responsible for IFN-γ-dependent intestinal inflammation and Paneth cell loss, where T-bet-dependent ILC1 cells play a minor role in driving the parasite-induced immunopathology. This was evident from the analysis of T-bet deficiency that did not prevent the intestinal inflammation and instead revealed that T-bet-deficient CD4+ Th1 cells are sufficient for T. gondii-triggered acute ileitis and Paneth cell loss. These results revealed that T-bet independent Th1 effector cells are major functional mediators of the type I immunopathological response during acute gastrointestinal infection.
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