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Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells
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...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9966443/ https://www.ncbi.nlm.nih.gov/pubmed/36839525 http://dx.doi.org/10.3390/pathogens12020253 |
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author | Ahmadpour, Ehsan Babaie, Farhad Kazemi, Tohid Mehrani Moghaddam, Sirous Moghimi, Ata Hosseinzadeh, Ramin Nissapatorn, Veeranoot Pagheh, Abdol Sattar |
author_facet | Ahmadpour, Ehsan Babaie, Farhad Kazemi, Tohid Mehrani Moghaddam, Sirous Moghimi, Ata Hosseinzadeh, Ramin Nissapatorn, Veeranoot Pagheh, Abdol Sattar |
author_sort | Ahmadpour, Ehsan |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-9966443 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99664432023-02-26 Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells Ahmadpour, Ehsan Babaie, Farhad Kazemi, Tohid Mehrani Moghaddam, Sirous Moghimi, Ata Hosseinzadeh, Ramin Nissapatorn, Veeranoot Pagheh, Abdol Sattar Pathogens Review 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. MDPI 2023-02-04 /pmc/articles/PMC9966443/ /pubmed/36839525 http://dx.doi.org/10.3390/pathogens12020253 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Ahmadpour, Ehsan Babaie, Farhad Kazemi, Tohid Mehrani Moghaddam, Sirous Moghimi, Ata Hosseinzadeh, Ramin Nissapatorn, Veeranoot Pagheh, Abdol Sattar Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells |
title | Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells |
title_full | Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells |
title_fullStr | Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells |
title_full_unstemmed | Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells |
title_short | Overview of Apoptosis, Autophagy, and Inflammatory Processes in Toxoplasma gondii Infected Cells |
title_sort | overview of apoptosis, autophagy, and inflammatory processes in toxoplasma gondii infected cells |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9966443/ https://www.ncbi.nlm.nih.gov/pubmed/36839525 http://dx.doi.org/10.3390/pathogens12020253 |
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