• 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

固有免疫在抗结核分枝杆菌感染的适应性免疫增强之前坚守侧翼防线。

Innate Immunity Holding the Flanks until Reinforced by Adaptive Immunity against Mycobacterium tuberculosis Infection.

作者信息

Khan Nargis, Vidyarthi Aurobind, Javed Shifa, Agrewala Javed N

机构信息

Council of Scientific and Industrial Research - Institute of Microbial Technology Chandigarh, India.

Department of Cytology and Gynecologic Pathology, Postgraduate Institute of Medical Education and Research Chandigarh, India.

出版信息

Front Microbiol. 2016 Mar 14;7:328. doi: 10.3389/fmicb.2016.00328. eCollection 2016.

DOI:10.3389/fmicb.2016.00328
PMID:27014247
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4789502/
Abstract

T cells play a cardinal role in imparting protection against Mycobacterium tuberculosis (Mtb). However, ample time is required before T-cells are able to evoke efficient effector responses in the lung, where the mycobacterium inflicts disease. This delay in T cells priming, which is termed as lag phase, provides sufficient time for Mtb to replicate and establish itself within the host. In contrast, innate immunity efficiently curb the growth of Mtb during initial phase of infection through several mechanisms. Pathogen recognition by innate cells rapidly triggers a cascade of events, such as apoptosis, autophagy, inflammasome formation and nitric oxide production to kill intracellular pathogens. Furthermore, bactericidal mechanisms such as autophagy and apoptosis, augment the antigen processing and presentation, thereby contributing substantially to the induction of adaptive immunity. This manuscript highlights the role of innate immune mechanisms in restricting the survival of Mtb during lag phase. Finally, this article provides new insight for designing immuno-therapies by targeting innate immune mechanisms to achieve optimum immune response to cure TB.

摘要

T细胞在提供针对结核分枝杆菌(Mtb)的保护方面起着关键作用。然而,在T细胞能够在肺部引发有效的效应反应之前,需要充足的时间,而肺部正是分枝杆菌引发疾病的部位。T细胞启动的这种延迟,即所谓的滞后阶段,为Mtb在宿主体内复制并立足提供了充足的时间。相比之下,固有免疫在感染初期通过多种机制有效地抑制Mtb的生长。固有细胞对病原体的识别迅速触发一系列事件,如细胞凋亡、自噬、炎性小体形成和一氧化氮产生,以杀死细胞内病原体。此外,诸如自噬和细胞凋亡等杀菌机制增强了抗原加工和呈递,从而对适应性免疫的诱导做出了重大贡献。本手稿强调了固有免疫机制在滞后阶段限制Mtb存活中的作用。最后,本文通过靶向固有免疫机制以实现治愈结核病的最佳免疫反应,为设计免疫疗法提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7193/4789502/4443e6a67b5c/fmicb-07-00328-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7193/4789502/4443e6a67b5c/fmicb-07-00328-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7193/4789502/4443e6a67b5c/fmicb-07-00328-g001.jpg

相似文献

1
Innate Immunity Holding the Flanks until Reinforced by Adaptive Immunity against Mycobacterium tuberculosis Infection.固有免疫在抗结核分枝杆菌感染的适应性免疫增强之前坚守侧翼防线。
Front Microbiol. 2016 Mar 14;7:328. doi: 10.3389/fmicb.2016.00328. eCollection 2016.
2
[Frontier of mycobacterium research--host vs. mycobacterium].[分枝杆菌研究前沿——宿主与分枝杆菌]
Kekkaku. 2005 Sep;80(9):613-29.
3
[Protective immunity against Mycobacterium tuberculosis].[针对结核分枝杆菌的保护性免疫]
Kekkaku. 2006 Nov;81(11):687-91.
4
New insights into the evasion of host innate immunity by Mycobacterium tuberculosis.结核分枝杆菌逃避宿主固有免疫的新见解。
Cell Mol Immunol. 2020 Sep;17(9):901-913. doi: 10.1038/s41423-020-0502-z. Epub 2020 Jul 29.
5
Infection and Innate Responses in a New Model of Lung Alveolar Macrophages.肺泡巨噬细胞新型模型中的感染与固有免疫反应。
Front Immunol. 2018 Mar 12;9:438. doi: 10.3389/fimmu.2018.00438. eCollection 2018.
6
Distinct Strategies Employed by Dendritic Cells and Macrophages in Restricting Mycobacterium tuberculosis Infection: Different Philosophies but Same Desire.树突状细胞和巨噬细胞在限制结核分枝杆菌感染中采用的不同策略:理念不同但目标一致。
Int Rev Immunol. 2016 Sep 2;35(5):386-398. doi: 10.3109/08830185.2015.1015718. Epub 2015 Mar 20.
7
Bag it, tag it: ubiquitin ligases and host resistance to Mycobacterium tuberculosis.包裹它,标记它:泛素连接酶和宿主对结核分枝杆菌的抗性。
Trends Microbiol. 2022 Oct;30(10):973-985. doi: 10.1016/j.tim.2022.03.010. Epub 2022 Apr 29.
8
Innate Immune Defenses in Human Tuberculosis: An Overview of the Interactions between Mycobacterium tuberculosis and Innate Immune Cells.人体结核病的固有免疫防御:结核分枝杆菌与固有免疫细胞相互作用概述。
J Immunol Res. 2015;2015:747543. doi: 10.1155/2015/747543. Epub 2015 Jul 14.
9
Mycobacterial Lipoprotein Z Triggers Efficient Innate and Adaptive Immunity for Protection Against Infection.分枝杆菌脂蛋白 Z 触发有效的先天和适应性免疫,以预防感染。
Front Immunol. 2019 Jan 16;9:3190. doi: 10.3389/fimmu.2018.03190. eCollection 2018.
10
Autophagy as an innate defense against mycobacteria.自噬作为先天防御对抗分枝杆菌。
Pathog Dis. 2013 Mar;67(2):108-18. doi: 10.1111/2049-632X.12023. Epub 2013 Feb 21.

引用本文的文献

1
LILRB1-HLA-G axis defines a checkpoint driving natural killer cell exhaustion in tuberculosis.LILRB1-HLA-G 轴定义了一个检查点,驱动结核分枝杆菌自然杀伤细胞衰竭。
EMBO Mol Med. 2024 Aug;16(8):1755-1790. doi: 10.1038/s44321-024-00106-1. Epub 2024 Jul 19.
2
Advanced drug delivery and therapeutic strategies for tuberculosis treatment.用于结核病治疗的先进药物输送和治疗策略。
J Nanobiotechnology. 2023 Nov 9;21(1):414. doi: 10.1186/s12951-023-02156-y.
3
Initial immune response after exposure to or to SARS-COV-2: similarities and differences.

本文引用的文献

1
Signaling through NOD-2 and TLR-4 Bolsters the T cell Priming Capability of Dendritic cells by Inducing Autophagy.通过NOD-2和TLR-4发出的信号,通过诱导自噬增强树突状细胞的T细胞启动能力。
Sci Rep. 2016 Jan 12;6:19084. doi: 10.1038/srep19084.
2
NOD-2 and TLR-4 Signaling Reinforces the Efficacy of Dendritic Cells and Reduces the Dose of TB Drugs against Mycobacterium tuberculosis.NOD-2和TLR-4信号增强树突状细胞的功效并降低抗结核分枝杆菌的结核病药物剂量。
J Innate Immun. 2016;8(3):228-42. doi: 10.1159/000439591. Epub 2015 Nov 28.
3
Innate Immune Defenses in Human Tuberculosis: An Overview of the Interactions between Mycobacterium tuberculosis and Innate Immune Cells.
初次免疫应答:接触 或 SARS-COV-2 后的异同。
Front Immunol. 2023 Aug 17;14:1244556. doi: 10.3389/fimmu.2023.1244556. eCollection 2023.
4
Comprehensive Analysis of RELL2 as a Potential Biomarker Associated with Tumor Immune Infiltrating Cells in a Pan-Cancer Analysis.RELL2 作为一种潜在的与泛癌分析中肿瘤免疫浸润细胞相关的生物标志物的全面分析。
Dis Markers. 2022 May 18;2022:5009512. doi: 10.1155/2022/5009512. eCollection 2022.
5
The Research Progress in Immunotherapy of Tuberculosis.结核病免疫治疗的研究进展。
Front Cell Infect Microbiol. 2021 Nov 15;11:763591. doi: 10.3389/fcimb.2021.763591. eCollection 2021.
6
Serum levels of inhibitory costimulatory molecules and correlations with levels of innate immune cytokines in patients with pulmonary tuberculosis.肺结核患者血清抑制性共刺激分子水平与固有免疫细胞因子水平的相关性。
J Int Med Res. 2021 Aug;49(8):3000605211036832. doi: 10.1177/03000605211036832.
7
TLRs in Mycobacterial Pathogenesis: Black and White or Shades of Gray.TLRs 在分枝杆菌发病机制中的作用:非黑即白,还是亦黑亦白?
Curr Microbiol. 2021 Jun;78(6):2183-2193. doi: 10.1007/s00284-021-02488-8. Epub 2021 Apr 12.
8
Albumin fusion with granulocyte-macrophage colony-stimulating factor acts as an immunotherapy against chronic tuberculosis.白蛋白与粒细胞-巨噬细胞集落刺激因子融合可作为一种免疫疗法,用于治疗慢性结核病。
Cell Mol Immunol. 2021 Oct;18(10):2393-2401. doi: 10.1038/s41423-020-0439-2. Epub 2020 May 7.
9
Invasion of the Human Lung: First Contact.人类肺部的侵袭:首次接触。
Front Immunol. 2018 Jun 12;9:1346. doi: 10.3389/fimmu.2018.01346. eCollection 2018.
10
Deviant Behavior: Tick-Borne Pathogens and Inflammasome Signaling.异常行为:蜱传病原体与炎性小体信号传导
Vet Sci. 2016 Sep 28;3(4):27. doi: 10.3390/vetsci3040027.
人体结核病的固有免疫防御:结核分枝杆菌与固有免疫细胞相互作用概述。
J Immunol Res. 2015;2015:747543. doi: 10.1155/2015/747543. Epub 2015 Jul 14.
4
Autophagy in the fight against tuberculosis.自噬在对抗结核病中的作用
DNA Cell Biol. 2015 Apr;34(4):228-42. doi: 10.1089/dna.2014.2745. Epub 2015 Jan 21.
5
Triggering through Toll-like receptor 2 limits chronically stimulated T-helper type 1 cells from undergoing exhaustion.通过Toll样受体2触发可限制长期受刺激的1型辅助性T细胞发生耗竭。
J Infect Dis. 2015 Feb 1;211(3):486-96. doi: 10.1093/infdis/jiu472. Epub 2014 Aug 25.
6
Apoptotic neutrophils augment the inflammatory response to Mycobacterium tuberculosis infection in human macrophages.凋亡中性粒细胞增强人巨噬细胞感染结核分枝杆菌的炎症反应。
PLoS One. 2014 Jul 7;9(7):e101514. doi: 10.1371/journal.pone.0101514. eCollection 2014.
7
Bacteria-autophagy interplay: a battle for survival.细菌自噬相互作用:生存之战。
Nat Rev Microbiol. 2014 Feb;12(2):101-14. doi: 10.1038/nrmicro3160. Epub 2014 Jan 2.
8
Autophagy and human diseases.自噬与人类疾病。
Cell Res. 2014 Jan;24(1):69-79. doi: 10.1038/cr.2013.161. Epub 2013 Dec 10.
9
Mycobacterium tuberculosis and the host cell inflammasome: a complex relationship.结核分枝杆菌与宿主细胞炎性小体:一种复杂的关系。
Front Cell Infect Microbiol. 2013 Oct 9;3:62. doi: 10.3389/fcimb.2013.00062. eCollection 2013.
10
Mycobacterium tuberculosis infection of human dendritic cells decreases integrin expression, adhesion and migration to chemokines.结核分枝杆菌感染人树突状细胞后会降低整合素的表达,进而影响其对趋化因子的黏附和迁移。
Immunology. 2014 Jan;141(1):39-51. doi: 10.1111/imm.12164.