Innate and acquired immune responses to mycobacterial infections: involvement of IL-17A/IL-23 axis in protective immunity.

Q4 Medicine
Masayuki Umemura, Goro Matsuzaki
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引用次数: 5

Abstract

Pulmonary tuberculosis is an infectious disease caused by Mycobacterium tuberculosis, and continues to be a serious threat to human life. Since M. tuberculosis establishes intracellular parasitism in macrophages, host innate and acquired immune systems have to detect and enhance bactericidal activity against the intracellular bacteria. Understanding of interaction between pathogenic factors of M. tuberculosis and host is also important to understand how immune system copes with the pathogen. In this review, we shortly summarize the mechanisms how innate and acquired immunity recognize M. tuberculosis or M. tuberculosis-infected cells and protects hosts from the infection. Furthermore, IL-17A/IL-23 axis, a recently focused inflammatory cytokine system, is discussed in the context of anti-mycobacterial protective immunity.

对分枝杆菌感染的先天和获得性免疫反应:IL-17A/IL-23轴参与保护性免疫
肺结核是由结核分枝杆菌引起的一种传染病,一直严重威胁着人类的生命。由于结核分枝杆菌在巨噬细胞中建立细胞内寄生,宿主先天和获得性免疫系统必须检测并增强对细胞内细菌的杀菌活性。了解结核分枝杆菌致病因子与宿主之间的相互作用对于了解免疫系统如何应对病原体也很重要。本文就先天免疫和获得性免疫识别结核分枝杆菌或结核分枝杆菌感染细胞并保护宿主免受感染的机制作一综述。此外,IL-17A/IL-23轴是最近关注的炎症细胞因子系统,在抗分枝杆菌保护性免疫的背景下进行了讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Japanese Journal of Leprosy
Japanese Journal of Leprosy Medicine-Dermatology
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