Parasite-induced TH1 cells and intestinal dysbiosis cooperate in IFN-γ-dependent elimination of Paneth cells.
Parasite-induced TH1 cells and intestinal dysbiosis cooperate in IFN-γ-dependent elimination of Paneth cells.
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病原体激活Toll样受体（TLR）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，我们表明，IFN-γ的生产过程中的粘膜反应的原生动物寄生虫弓形虫的CD 4 + TH 1细胞的结果在生态失调和潘氏细胞的消除。潘氏细胞死亡导致抗微生物肽的损失，并与革兰氏阴性细菌的肠杆菌科家族的不受控制的扩增一起发生。寄生虫引起的肠道病理需要扩张的肠道细菌。T.弓形虫感染鉴定了T细胞固有TLR途径作为CD 4 + T细胞中IFN-γ产生的主要调节剂，其负责潘氏细胞死亡、生态失调和肠道免疫病理学。
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+ TH1 cells during mucosal responses to the protozoan parasite Toxoplasma gondii results 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 TH1 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.
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影响因子：
30.3
作者：
Benson A;Pifer R;Behrendt CL;Hooper LV;Yarovinsky F
通讯作者：
Yarovinsky F
影响因子：
32.4
作者：
Hou, Baidong;Reizis, Boris;DeFranco, Anthony L.
通讯作者：
DeFranco, Anthony L.
影响因子：
8.7
作者：
Beutler B
通讯作者：
Beutler B
影响因子：
32.4
作者：
Hou B;Saudan P;Ott G;Wheeler ML;Ji M;Kuzmich L;Lee LM;Coffman RL;Bachmann MF;DeFranco AL
通讯作者：
DeFranco AL
影响因子：
32.4
作者：
Jankovic, D;Kullberg, MC;Sher, A
通讯作者：
Sher, A