Notch 1 Is Involved in CD4(+) T Cell Differentiation Into Th1 Subtype During Helicobacter pylori Infection.
Notch 1 Is Involved in CD4(+) T Cell Differentiation Into Th1 Subtype During Helicobacter pylori Infection.
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Notch 1 参与幽门螺杆菌感染期间 CD4(+) T 细胞分化为 Th1 亚型。
DOI：
10.3389/fcimb.2020.575271
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发表时间：
2020
影响因子：
5.7
通讯作者：
Li Y
中科院分区：
文献类型：
--
作者：
Xie J;Wen J;Chen C;Luo M;Hu B;Wu D;Ye J;Lin Y;Ning L;Ning Y;Li Y
幽门螺杆菌感染诱导CD 4 + T细胞分化为产生IFN-γ的Th 1细胞。然而，这一过程背后的机制细节仍不清楚。Notch信号通路在许多Th 1介导的炎症性疾病中调节CD 4 + T细胞向Th 1亚型的分化，但在H.幽门感染本研究探讨了H.使用人类信号转导通路RTPRT 2 Profiler PCR阵列，幽门螺杆菌感染患者与健康对照的差异，并且这种改变与Notch信号通路相关，如Bioinformation分析的。实时荧光定量PCR结果显示，Notch 1及其靶基因Hes-1在H.与健康对照组相比，幽门螺杆菌感染的个体增加。此外，Th 1主转录因子T-bet和Th 1特征性细胞因子IFN-γ的mRNA表达在H.幽门螺杆菌感染的个体，并与Notch 1的表达呈正相关。Notch 1和IFN-γ蛋白水平在H.通过流式细胞术和ELISA确认的幽门螺杆菌感染的个体。在体外，抑制Notch信号通路可降低Notch 1、Hes-1、T-bet和IFN-γ的mRNA表达，并降低Notch 1和IFN-γ的蛋白水平及IFN-γ的分泌。幽门。总的来说，这是第一个证据表明Notch 1在H. pylori感染，这将有助于利用Notch 1作为控制H.幽门感染
Helicobacter pylori infection induces CD4+ T differentiation cells into IFN-γ-producing Th1 cells. However, the details of mechanism underlying this process remain unclear. Notch signal pathway has been reported to regulate the differentiation of CD4+ T cells into Th1 subtype in many Th1-mediated inflammatory disorders but not yet in H. pylori infection. In the present study, the mRNA expression pattern of CD4+ T cells in H. pylori–infected patients differed from that of healthy control using Human Signal Transduction Pathway Finder RT2 Profiler PCR Array, and this alteration was associated with Notch signal pathway, as analyzed by Bioinformation. Quantitative real-time PCR showed that the mRNA expression of Notch1 and its target gene Hes-1 in CD4+ T cells of H. pylori–infected individuals increased compared with the healthy controls. In addition, the mRNA expression of Th1 master transcription factor T-bet and Th1 signature cytokine IFN-γ was both upregulated in H. pylori–infected individuals and positively correlated with Notch1 expression. The increased protein level of Notch1 and IFN-γ were also observed in H. pylori–infected individuals confirmed by flow cytometry and ELISA. In vitro, inhibition of Notch signaling decreased the mRNA expression of Notch1, Hes-1, T-bet, and IFN-γ, and reduced the protein levels of Notch1 and IFN-γ and the secretion of IFN-γ in CD4+ T cells stimulated by H. pylori. Collectively, this is the first evidence that Notch1 is upregulated and involved in the differentiation of Th1 cells during H. pylori infection, which will facilitate exploiting Notch1 as a therapeutic target for the control of H. pylori infection.
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影响因子：
2.1
作者：
Jiao, Z.;Wang, W.;Li, J.
通讯作者：
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影响因子：
4.4
作者：
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通讯作者：
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影响因子：
5.8
作者：
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通讯作者：
Del Prete, G
影响因子：
4.6
作者：
Furukawa T;Ishifune C;Tsukumo SI;Hozumi K;Maekawa Y;Matsui N;Kaji R;Yasutomo K
通讯作者：
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影响因子：
3.1
作者：
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通讯作者：
Eaton, Kathryn A.