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首页> 外文期刊>Nature immunology >Parasite-induced T H 1 cells and intestinal dysbiosis cooperate in IFN-γ-dependent elimination of Paneth cells
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Parasite-induced T H 1 cells and intestinal dysbiosis cooperate in IFN-γ-dependent elimination of Paneth cells

机译：寄生虫诱导的T H 1细胞和肠道营养不良共同影响IFN-γ依赖性Paneth细胞的消除

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摘要

Activation of Toll-like receptors (TLRs) by pathogens triggers cytokine production and T cell activation, immune defense mechanisms that are linked to immunopathology. Here we show that IFN-γ production by CD4 + T H 1 cells during mucosal responses to the protozoan parasite Toxoplasma gondii resulted in dysbiosis and the elimination of Paneth cells. Paneth cell death led to loss of antimicrobial peptides and occurred in conjunction with uncontrolled expansion of the Enterobacteriaceae family of Gram-negative bacteria. The expanded intestinal bacteria were required for the parasite-induced intestinal pathology. The investigation of cell type-specific factors regulating T H 1 polarization during T. gondii infection identified the T cell-intrinsic TLR pathway as a major regulator of IFN-γ production in CD4 + T cells responsible for Paneth cell death, dysbiosis and intestinal immunopathology.
机译：病原体激活Toll样受体（TLR）会触发细胞因子产生和T细胞活化，这是与免疫病理学相关的免疫防御机制。在这里，我们显示CD4 + T H 1细胞在对原生动物寄生虫弓形虫的粘膜反应过程中产生IFN-γ导致营养不良和Paneth细胞的消除。 Paneth细胞死亡导致抗菌肽丢失，并与革兰氏阴性菌肠杆菌科家族的失控扩张有关。寄生虫诱导的肠病理需要扩张的肠细菌。刚地弓形虫感染期间调节T H 1极化的细胞类型特异性因素的研究确定，T细胞内在性TLR途径是负责Paneth细胞死亡，营养不良和肠道免疫病理的CD4 + T细胞中IFN-γ产生的主要调节剂。

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