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 group 1 innate lymphoid cells have 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.

中文翻译：

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T-bet 独立 Th1 反应在弓形虫感染期间诱导肠道免疫病理学。

先天性和适应性免疫细胞协调产生 IFN-γ 是宿主防御的核心，但也可以引发免疫病理学。在弓形虫感染期间淋巴样细胞对 IFN-γ 介导的肠道病理学的特异性贡献的研究确定 CD4+ T 细胞是导致 IFN-γ 依赖性肠道炎症和潘氏细胞丢失的关键细胞群，其中 T-bet-依赖组 1 先天性淋巴样细胞在驱动寄生虫诱导的免疫病理学中起次要作用。这从 T-bet 缺陷分析中可以明显看出，T-bet 缺陷并不能预防肠道炎症，而是表明 T-bet 缺陷型 CD4+ Th1 细胞足以应对弓形虫引发的急性回肠炎和潘氏细胞丢失。