Innate type 1 immune response, but not IL-17 cells control tuberculosis infection.
IL-1
IL-17 blockade
Innate immunity
Interferons
Mycobacterial infection
TNF
Journal
Biomedical journal
ISSN: 2320-2890
Titre abrégé: Biomed J
Pays: United States
ID NLM: 101599820
Informations de publication
Date de publication:
04 2021
04 2021
Historique:
received:
28
04
2020
revised:
16
06
2020
accepted:
29
06
2020
pubmed:
17
8
2020
medline:
28
9
2021
entrez:
17
8
2020
Statut:
ppublish
Résumé
The role of the innate immune response and host resistance to Mycobacterium tuberculosis infection (TB) is reviewed. Based on our data and the abundant literature, an early type 1 immune response is critical for infection control, while ILC3 and Th17 cells seem to be dispensable. Indeed, in M. tuberculosis infected mice, transcriptomic levels of Il17, Il17ra, Il22 and Il23a were not significantly modified as compared to controls, suggesting a limited role of IL-17 and IL-22 pathways in TB infection control. Neutralization of IL-17A or IL-17F did not affect infection control either. Ongoing clinical studies with IL-17 neutralizing antibodies show high efficacy in patients with psoriasis without increased incidence of TB infection or reactivation. Therefore, both experimental studies in mice and clinical trials in human patients suggest no risk of TB infection or reactivation by therapeutic IL-17 antibodies, unlike by TNF.
Identifiants
pubmed: 32798210
pii: S2319-4170(20)30097-4
doi: 10.1016/j.bj.2020.06.011
pmc: PMC8178558
pii:
doi:
Substances chimiques
Interleukin-17
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
165-171Informations de copyright
Copyright © 2020 Chang Gung University. Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Conflicts of Interest The authors declare no conflict of interest.
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