生物学杂志

生物学杂志 ›› 2022, Vol. 39 ›› Issue (4): 94-.doi: 10.3969/j.issn. 2095-1736.2022.04.094

• 综述与专论 • 上一篇    下一篇

结核分枝杆菌诱导宿主Ⅰ型干扰素应答及其免疫调控功能研究进展

  

  1. 1. 扬州大学 江苏省人兽共患病学重点实验室/江苏省动物重要疫病与人兽共患病防控协同创新中心，
    扬州 225009；
    2. 扬州大学 农业农村部农产品质量安全生物性危害因子（动物源）控制重点实验室， 扬州 225009
  • 出版日期:2022-08-18 发布日期:2022-08-15
  • 通讯作者: 徐正中，博士，副教授，研究方向为微生物与免疫学，E-mail: zzxu@yzu.edu.cn；焦新安，博士，教授，研究方向为人兽共患病学，E-mail: jiao@yzu.edu.cn
  • 作者简介:姚志鸿，硕士研究生，研究方向为生物工程，E-mail: 479094192@qq.com
  • 基金资助:
    江苏省自然科学基金项目（BK20201432）； 扬州大学科技创新培育基金项目（2019CXJ158）； 江苏“六大人才高峰”项目（SWYY-083）； 优势学科建设工程项目（PAPD）

Progress of Mycobacterium tuberculosis inducing host type I interferon response and immunoregulatory function

  1. 1. Jiangsu Key Lab of Zoonosis/Jiangsu Co-Innovation Center for Prevention and Control of Important Animal
    Infectious Diseases and Zoonoses, Yangzhou University, Yangzhou 225009, China;
    2. Key Laboratory of Prevention and Control of Biological Hazard Factors (Animal Origin) for Agrifood Safety and
    Quality, MOA of China, Yangzhou University, Yangzhou 225009, China
  • Online:2022-08-18 Published:2022-08-15

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摘要： 阐述结核分枝杆菌感染过程中I型干扰素的免疫功能，I型干扰素既可以作为活动性结核的标识并加剧结核致病过程，同时也参与机体的抗结核免疫防御过程并降低结核分枝杆菌胞内存活。另外，在不同层面归纳结核分枝杆菌感染诱导宿主I型干扰素表达及信号通路活化的机制，并探讨结核分枝杆菌可以通过调控I型干扰素应答水平以逃逸宿主免疫，从而促进其在宿主体内持续感染。旨在总结结核分枝杆菌诱导宿主Ⅰ型干扰素应答及其免疫调控功能的研究进展，进而为抗结核药物靶标筛选及疫苗研制提供新思路。

关键词: 结核病, 结核分枝杆菌, Ⅰ型干扰素, 免疫调控, 免疫逃逸

Abstract: This paper summarizes the immune regulation function of type I interferon in the process of Mycobacterium tuberculosis infection. Type I interferon can be used as a marker of active tuberculosis and aggravate the pathogenic process of tuberculosis. At the same time, type I interferon also participates in the immune defense process of anti-tuberculosis and effectively reduces the intracellular survival of Mycobacterium tuberculosis. In addition, this paper summarizes the mechanism of host type I interferon expression and signal pathway activation induced by Mycobacterium tuberculosis infection at different levels, and discussed that some components of Mycobacterium tuberculosis can escape host immunity by regulating the response level of type I interferon, so as to promote its survival in the host. The purpose of this paper is to summarize the research progress of host type I interferon response induced by Mycobacterium tuberculosis and its immunomodulatory function, so as to provide new ideas for the screening of anti-tuberculosis drug targets and the development of vaccines in the future.

Key words: tuberculosis, Mycobacterium tuberculosis, type I interferon, immunoregulation, immune escape

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