• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Systems-wide analyses of mucosal immune responses to Helicobacter pylori at the interface between pathogenicity and symbiosis.在致病性与共生关系界面上对幽门螺杆菌黏膜免疫反应的全系统分析。
Gut Microbes. 2016;7(1):3-21. doi: 10.1080/19490976.2015.1116673.
2
The role of T helper 1-cell response in Helicobacter pylori-infection.辅助性 T 细胞 1 型应答在幽门螺杆菌感染中的作用。
Microb Pathog. 2018 Oct;123:1-8. doi: 10.1016/j.micpath.2018.06.033. Epub 2018 Jun 21.
3
The Effects of Infection on Microbiota Associated With Gastric Mucosa and Immune Factors in Children.感染对儿童胃黏膜相关菌群及免疫因子的影响。
Front Immunol. 2021 Mar 24;12:625586. doi: 10.3389/fimmu.2021.625586. eCollection 2021.
4
Recruitment of CCR6 Foxp3 regulatory gastric infiltrating lymphocytes in Helicobacter pylori gastritis.招募 CCR6 Foxp3 调节性胃浸润淋巴细胞在幽门螺杆菌胃炎中的作用。
Helicobacter. 2019 Feb;24(1):e12550. doi: 10.1111/hel.12550. Epub 2018 Nov 9.
5
Bacterial factors and immune pathogenesis in Helicobacter pylori infection.幽门螺杆菌感染中的细菌因素与免疫发病机制
Gut. 1998 Jul;43 Suppl 1(Suppl 1):S2-5.
6
GITR Promotes the Polarization of TFH-Like Cells in -Positive Gastritis.GITR 促进 + 阳性胃炎中滤泡辅助样 T 细胞的极化。
Front Immunol. 2021 Sep 10;12:736269. doi: 10.3389/fimmu.2021.736269. eCollection 2021.
7
The crosstalk between H. pylori virulence factors and the PD1:PD-L1 immune checkpoint inhibitors in progression to gastric cancer.幽门螺杆菌毒力因子与 PD1:PD-L1 免疫检查点抑制剂在胃癌进展中的相互作用。
Immunol Lett. 2021 Nov;239:1-11. doi: 10.1016/j.imlet.2021.06.009. Epub 2021 Aug 5.
8
CCR6 T helper cells and regulatory T cells in the blood and gastric mucosa during Helicobacter pylori infection.在幽门螺杆菌感染期间,血液和胃黏膜中的 CCR6 T 辅助细胞和调节性 T 细胞。
Helicobacter. 2024 May-Jun;29(3):e13097. doi: 10.1111/hel.13097.
9
gammadelta T cells increase with gastric mucosal interleukin (IL)-7, IL-1beta, and Helicobacter pylori urease specific immunoglobulin levels via CCR2 upregulation in Helicobacter pylori gastritis.在幽门螺杆菌胃炎中,γδ T细胞通过CCR2上调,随胃黏膜白细胞介素(IL)-7、IL-1β和幽门螺杆菌脲酶特异性免疫球蛋白水平升高而增加。
J Gastroenterol Hepatol. 2006 Jan;21(1 Pt 1):32-40. doi: 10.1111/j.1440-1746.2005.04148.x.
10
Immune evasion strategies used by Helicobacter pylori.幽门螺杆菌采用的免疫逃避策略。
World J Gastroenterol. 2014 Sep 28;20(36):12753-66. doi: 10.3748/wjg.v20.i36.12753.

引用本文的文献

1
Pivotal role of virulence genes in pathogenicity and vaccine development.毒力基因在致病性和疫苗开发中的关键作用。
Front Med (Lausanne). 2025 Jan 6;11:1523991. doi: 10.3389/fmed.2024.1523991. eCollection 2024.
2
Long-term Helicobacter pylori infection is associated with an increased risk of carotid plaque formation: a retrospective cohort study.长期幽门螺杆菌感染与颈动脉斑块形成风险增加相关:一项回顾性队列研究。
Front Cardiovasc Med. 2024 Oct 24;11:1476435. doi: 10.3389/fcvm.2024.1476435. eCollection 2024.
3
Effects and mechanisms of infection on the occurrence of extra-gastric tumors.感染对胃外肿瘤发生的影响及其机制。
World J Gastroenterol. 2024 Oct 7;30(37):4090-4103. doi: 10.3748/wjg.v30.i37.4090.
4
Current Knowledge about Gastric Microbiota with Special Emphasis on Related Gastric Conditions.关于胃微生物群的当前知识,特别强调相关胃部疾病
Curr Issues Mol Biol. 2024 May 20;46(5):4991-5009. doi: 10.3390/cimb46050299.
5
Helicobacter pylori disrupts gastric mucosal homeostasis by stimulating macrophages to secrete CCL3.幽门螺杆菌通过刺激巨噬细胞分泌 CCL3 破坏胃黏膜稳态。
Cell Commun Signal. 2024 May 10;22(1):263. doi: 10.1186/s12964-024-01627-5.
6
Strategies of in evading host innate and adaptive immunity: insights and prospects for therapeutic targeting.逃避宿主固有免疫和适应性免疫的策略:治疗靶点的见解与前景
Front Cell Infect Microbiol. 2024 Feb 26;14:1342913. doi: 10.3389/fcimb.2024.1342913. eCollection 2024.
7
Targeting the blood-brain barrier to delay aging-accompanied neurological diseases by modulating gut microbiota, circadian rhythms, and their interplays.通过调节肠道微生物群、昼夜节律及其相互作用来靶向血脑屏障,以延缓衰老相关的神经疾病。
Acta Pharm Sin B. 2023 Dec;13(12):4667-4687. doi: 10.1016/j.apsb.2023.08.009. Epub 2023 Aug 14.
8
Gastric microbiota dysbiosis and infection.胃微生物群失调与感染。
Front Microbiol. 2023 Mar 30;14:1153269. doi: 10.3389/fmicb.2023.1153269. eCollection 2023.
9
The Roles of Innate Lymphoid Cells in the Gastric Mucosal Immunology and Oncogenesis of Gastric Cancer.固有淋巴细胞在胃癌胃黏膜免疫和发生中的作用。
Int J Mol Sci. 2023 Apr 2;24(7):6652. doi: 10.3390/ijms24076652.
10
and Autoimmune Diseases: Involving Multiple Systems.以及自身免疫性疾病:涉及多个系统。
Front Immunol. 2022 Feb 10;13:833424. doi: 10.3389/fimmu.2022.833424. eCollection 2022.

本文引用的文献

1
Bistability analyses of CD4+ T follicular helper and regulatory cells during Helicobacter pylori infection.幽门螺杆菌感染期间CD4 +滤泡辅助性T细胞和调节性T细胞的双稳态分析
J Theor Biol. 2016 Jun 7;398:74-84. doi: 10.1016/j.jtbi.2016.02.036. Epub 2016 Mar 3.
2
Pathogenesis of Helicobacter pylori Infection.幽门螺杆菌感染的发病机制
Helicobacter. 2015 Sep;20 Suppl 1(0 1):8-16. doi: 10.1111/hel.12251.
3
Modeling the Regulatory Mechanisms by Which NLRX1 Modulates Innate Immune Responses to Helicobacter pylori Infection.模拟NLRX1调节对幽门螺杆菌感染的先天免疫反应的调控机制。
PLoS One. 2015 Sep 14;10(9):e0137839. doi: 10.1371/journal.pone.0137839. eCollection 2015.
4
Helicobacter pylori CheZ(HP) and ChePep form a novel chemotaxis-regulatory complex distinct from the core chemotaxis signaling proteins and the flagellar motor.幽门螺杆菌CheZ(HP)和ChePep形成一种新型趋化性调节复合物,不同于核心趋化性信号蛋白和鞭毛马达。
Mol Microbiol. 2015 Sep;97(6):1063-78. doi: 10.1111/mmi.13086. Epub 2015 Jul 4.
5
Suppression of NLRX1 in chronic obstructive pulmonary disease.慢性阻塞性肺疾病中NLRX1的抑制作用
J Clin Invest. 2015 Jun;125(6):2458-62. doi: 10.1172/JCI71747. Epub 2015 May 4.
6
Helicobacter pylori-specific protection against inflammatory bowel disease requires the NLRP3 inflammasome and IL-18.幽门螺杆菌对炎症性肠病的特异性保护作用需要NLRP3炎性小体和白细胞介素-18。
Inflamm Bowel Dis. 2015 Apr;21(4):854-61. doi: 10.1097/MIB.0000000000000318.
7
OX40- and CD27-mediated costimulation synergizes with anti-PD-L1 blockade by forcing exhausted CD8+ T cells to exit quiescence.OX40和CD27介导的共刺激通过促使耗竭的CD8 + T细胞退出静止状态,与抗PD-L1阻断协同作用。
J Immunol. 2015 Jan 1;194(1):125-133. doi: 10.4049/jimmunol.1401644. Epub 2014 Nov 17.
8
Crosstalks between cytokines and Sonic Hedgehog in Helicobacter pylori infection: a mathematical model.幽门螺杆菌感染中细胞因子与音猬因子之间的相互作用:一个数学模型
PLoS One. 2014 Nov 3;9(11):e111338. doi: 10.1371/journal.pone.0111338. eCollection 2014.
9
Computational modeling of heterogeneity and function of CD4+ T cells.CD4+ T 细胞异质性与功能的计算建模。
Front Cell Dev Biol. 2014 Jul 29;2:31. doi: 10.3389/fcell.2014.00031. eCollection 2014.
10
Cytokine BAFF released by Helicobacter pylori-infected macrophages triggers the Th17 response in human chronic gastritis.幽门螺杆菌感染的巨噬细胞释放的细胞因子BAFF触发人类慢性胃炎中的Th17反应。
J Immunol. 2014 Dec 1;193(11):5584-94. doi: 10.4049/jimmunol.1302865. Epub 2014 Oct 22.

在致病性与共生关系界面上对幽门螺杆菌黏膜免疫反应的全系统分析。

Systems-wide analyses of mucosal immune responses to Helicobacter pylori at the interface between pathogenicity and symbiosis.

作者信息

Kronsteiner Barbara, Bassaganya-Riera Josep, Philipson Casandra, Viladomiu Monica, Carbo Adria, Abedi Vida, Hontecillas Raquel

机构信息

a Nutritional Immunology and Molecular Medicine Laboratory and Center for Modeling Immunity to Enteric Pathogens; Virginia Bioinformatics Institute; Virginia Tech ; Blacksburg , VA , USA.

b BioTherapeutics ; Blacksburg , VA , USA.

出版信息

Gut Microbes. 2016;7(1):3-21. doi: 10.1080/19490976.2015.1116673.

DOI:10.1080/19490976.2015.1116673
PMID:26939848
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4856448/
Abstract

Helicobacter pylori is the dominant member of the gastric microbiota in over half of the human population of which 5-15% develop gastritis or gastric malignancies. Immune responses to H. pylori are characterized by mixed T helper cell, cytotoxic T cell and NK cell responses. The presence of Tregs is essential for the control of gastritis and together with regulatory CX3CR1+ mononuclear phagocytes and immune-evasion strategies they enable life-long persistence of H. pylori. This H. pylori-induced regulatory environment might contribute to its cross-protective effect in inflammatory bowel disease and obesity. Here we review host-microbe interactions, the development of pro- and anti-inflammatory immune responses and how the latter contribute to H. pylori's role as beneficial member of the gut microbiota. Furthermore, we present the integration of existing and new data into a computational/mathematical model and its use for the investigation of immunological mechanisms underlying initiation, progression and outcomes of H. pylori infection.

摘要

幽门螺杆菌是超过半数人类胃微生物群中的主要成员,其中5%-15%的人会发展为胃炎或胃部恶性肿瘤。对幽门螺杆菌的免疫反应以混合性辅助性T细胞、细胞毒性T细胞和自然杀伤细胞反应为特征。调节性T细胞的存在对于控制胃炎至关重要,它们与调节性CX3CR1+单核吞噬细胞以及免疫逃避策略一起,使幽门螺杆菌能够终生持续存在。这种由幽门螺杆菌诱导的调节环境可能有助于其在炎症性肠病和肥胖症中的交叉保护作用。在这里,我们综述宿主-微生物相互作用、促炎和抗炎免疫反应的发展,以及后者如何促成幽门螺杆菌作为肠道微生物群有益成员的作用。此外,我们将现有数据和新数据整合到一个计算/数学模型中,并将其用于研究幽门螺杆菌感染的起始、进展和结局背后的免疫机制。