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Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy
Mycobacterium tuberculosis (M. tuberculosis) is the pathogen which causes tuberculosis (TB), a significant human public health threat. Co-infection of M. tuberculosis and the human immunodeficiency virus (HIV), emergence of drug resistant M. tuberculosis, and failure to develop highly effective TB v...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018485/ https://www.ncbi.nlm.nih.gov/pubmed/33666534 http://dx.doi.org/10.1080/22221751.2021.1899771 |
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author | Zhou, Jie Lv, Jingzhu Carlson, Chelsea Liu, Hui Wang, Hongtao Xu, Tao Wu, Fengjiao Song, Chuanwang Wang, Xiaojing Wang, Ting Qian, Zhongqing |
author_facet | Zhou, Jie Lv, Jingzhu Carlson, Chelsea Liu, Hui Wang, Hongtao Xu, Tao Wu, Fengjiao Song, Chuanwang Wang, Xiaojing Wang, Ting Qian, Zhongqing |
author_sort | Zhou, Jie |
collection | PubMed |
description | Mycobacterium tuberculosis (M. tuberculosis) is the pathogen which causes tuberculosis (TB), a significant human public health threat. Co-infection of M. tuberculosis and the human immunodeficiency virus (HIV), emergence of drug resistant M. tuberculosis, and failure to develop highly effective TB vaccines have limited control of the TB epidemic. Trained immunity is an enhanced innate immune response which functions independently of the adaptive/acquired immune system and responds non-specifically to reinfection with invading agents. Recently, several studies have found trained immunity has the capability to control and eliminate M. tuberculosis infection. Over the past decades, however, the consensus was adaptive immunity is the only protective mechanism by which hosts inhibit M. tuberculosis growth. Furthermore, autophagy plays an essential role in the development of trained immunity. Further investigation of trained immunity, M. tuberculosis infection, and the role of autophagy in this process provide new possibilities for vaccine development. In this review, we present the general characteristics of trained immunity and autophagy. We additionally summarize several examples where initiation of trained immunity contributes to the prevention of M. tuberculosis infection and propose future directions for research in this area. |
format | Online Article Text |
id | pubmed-8018485 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-80184852021-04-13 Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy Zhou, Jie Lv, Jingzhu Carlson, Chelsea Liu, Hui Wang, Hongtao Xu, Tao Wu, Fengjiao Song, Chuanwang Wang, Xiaojing Wang, Ting Qian, Zhongqing Emerg Microbes Infect Review Mycobacterium tuberculosis (M. tuberculosis) is the pathogen which causes tuberculosis (TB), a significant human public health threat. Co-infection of M. tuberculosis and the human immunodeficiency virus (HIV), emergence of drug resistant M. tuberculosis, and failure to develop highly effective TB vaccines have limited control of the TB epidemic. Trained immunity is an enhanced innate immune response which functions independently of the adaptive/acquired immune system and responds non-specifically to reinfection with invading agents. Recently, several studies have found trained immunity has the capability to control and eliminate M. tuberculosis infection. Over the past decades, however, the consensus was adaptive immunity is the only protective mechanism by which hosts inhibit M. tuberculosis growth. Furthermore, autophagy plays an essential role in the development of trained immunity. Further investigation of trained immunity, M. tuberculosis infection, and the role of autophagy in this process provide new possibilities for vaccine development. In this review, we present the general characteristics of trained immunity and autophagy. We additionally summarize several examples where initiation of trained immunity contributes to the prevention of M. tuberculosis infection and propose future directions for research in this area. Taylor & Francis 2021-03-30 /pmc/articles/PMC8018485/ /pubmed/33666534 http://dx.doi.org/10.1080/22221751.2021.1899771 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Zhou, Jie Lv, Jingzhu Carlson, Chelsea Liu, Hui Wang, Hongtao Xu, Tao Wu, Fengjiao Song, Chuanwang Wang, Xiaojing Wang, Ting Qian, Zhongqing Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy |
title | Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy |
title_full | Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy |
title_fullStr | Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy |
title_full_unstemmed | Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy |
title_short | Trained immunity contributes to the prevention of Mycobacterium tuberculosis infection, a novel role of autophagy |
title_sort | trained immunity contributes to the prevention of mycobacterium tuberculosis infection, a novel role of autophagy |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018485/ https://www.ncbi.nlm.nih.gov/pubmed/33666534 http://dx.doi.org/10.1080/22221751.2021.1899771 |
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