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- W4319317722 abstract "Toxoplasma gondii (T. gondii) is an obligate intracellular parasite. During the parasitic invasion, T. gondii creates a parasitophorous vacuole, which enables the modulation of cell functions, allowing its replication and host infection. It has effective strategies to escape the immune response and reach privileged immune sites and remain inactive in a controlled environment in tissue cysts. This current review presents the factors that affect host cells and the parasite, as well as changes in the immune system during host cell infection. The secretory organelles of T. gondii (dense granules, micronemes, and rhoptries) are responsible for these processes. They are involved with proteins secreted by micronemes and rhoptries (MIC, AMA, and RONs) that mediate the recognition and entry into host cells. Effector proteins (ROP and GRA) that modify the STAT signal or GTPases in immune cells determine their toxicity. Interference byhost autonomous cells during parasitic infection, gene expression, and production of microbicidal molecules such as reactive oxygen species (ROS) and nitric oxide (NO), result in the regulation of cell death. The high level of complexity in host cell mechanisms prevents cell death in its various pathways. Many of these abilities play an important role in escaping host immune responses, particularly by manipulating the expression of genes involved in apoptosis, necrosis, autophagy, and inflammation. Here we present recent works that define the mechanisms by which T. gondii interacts with these processes in infected host cells." @default.
- W4319317722 created "2023-02-08" @default.
- W4319317722 creator A5002590126 @default.
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- W4319317722 creator A5027119431 @default.
- W4319317722 creator A5041250136 @default.
- W4319317722 creator A5053687705 @default.
- W4319317722 date "2023-02-04" @default.
- W4319317722 modified "2023-10-02" @default.
- W4319317722 title "Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells" @default.
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