Zooming in on common immune evasion mechanisms of pathogens in phagolysosomes: potential broad-spectrum therapeutic targets against infectious diseases.
agonist
antagonist
apoptosis
drug target
intracellular pathogens
phagosomes
Journal
FEMS microbiology reviews
ISSN: 1574-6976
Titre abrégé: FEMS Microbiol Rev
Pays: England
ID NLM: 8902526
Informations de publication
Date de publication:
16 01 2023
16 01 2023
Historique:
received:
29
05
2022
revised:
06
10
2022
accepted:
18
10
2022
pubmed:
30
10
2022
medline:
19
1
2023
entrez:
29
10
2022
Statut:
ppublish
Résumé
The intracellular viral, bacterial, or parasitic pathogens evade the host immune challenges to propagate and cause fatal diseases. The microbes overpower host immunity at various levels including during entry into host cells, phagosome formation, phagosome maturation, phagosome-lysosome fusion forming phagolysosomes, acidification of phagolysosomes, and at times after escape into the cytosol. Phagolysosome is the final organelle in the phagocyte with sophisticated mechanisms to degrade the pathogens. The immune evasion strategies by the pathogens include the arrest of host cell apoptosis, decrease in reactive oxygen species, the elevation of Th2 anti-inflammatory response, avoidance of autophagy and antigen cross-presentation pathways, and escape from phagolysosomal killing. Since the phagolysosome organelle in relation to infection/cure is seldom discussed in the literature, we summarize here the common host as well as pathogen targets manipulated or utilized by the pathogens established in phagosomes and phagolysosomes, to hijack the host immune system for their benefit. These common molecules or pathways can be broad-spectrum therapeutic targets for drug development for intervention against infectious diseases caused by different intracellular pathogens.
Identifiants
pubmed: 36309472
pii: 6780197
doi: 10.1093/femsre/fuac041
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2022. Published by Oxford University Press on behalf of FEMS.