Loading…
Capers with caspases: Toxoplasma gondii tales of inflammation and survival
Intracellular pathogens strike a delicate balance between maintaining their survival within infected cells, while also activating host defense mechanisms. Toxoplasma gondii is a protozoan parasite that initiates a variety of host signaling pathways as it invades host cells and establishes residence...
Saved in:
Published in: | Current opinion in microbiology 2023-04, Vol.72, p.102264-102264, Article 102264 |
---|---|
Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Intracellular pathogens strike a delicate balance between maintaining their survival within infected cells, while also activating host defense mechanisms. Toxoplasma gondii is a protozoan parasite that initiates a variety of host signaling pathways as it invades host cells and establishes residence in a parasitophorous vacuole. Recent work has highlighted the interplay between T. gondii infection and innate immune pathways that lead to inflammation, several of which converge on caspases. This family of cysteine proteases function at the crossroads of inflammation and cell death and serve as a key target for parasite manipulation. This review focuses on the interaction of T. gondii with caspase-dependent inflammatory and cell death pathways and the role of parasite effector proteins in modulating these processes.
•During infection of innate immune cells, T. gondii activates caspase-1/11- and caspase-8-dependent inflammatory pathways.•T. gondii subverts the activity of apoptotic caspases within infected host cells, as a potential means of maintaining host cell survival and a replicative niche for the parasite.•Key parasite effector proteins function to maintain a balance between activating and inhibiting immune signaling pathways in infected cells. |
---|---|
ISSN: | 1369-5274 1879-0364 |
DOI: | 10.1016/j.mib.2023.102264 |