Advances in Toxoplasma gondii Treatment, Immunology and Host–Parasite Interaction

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: 31 July 2026 | Viewed by 529

Special Issue Editor


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Guest Editor
Section of Hematology-Oncology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA
Interests: malaria, toxoplasmosis, and leishmaniasis; host defense; immune response; nanoparticle based therapy

Special Issue Information

Dear Colleagues,

Toxoplasma gondii is an intracellular protozoan parasite. It infects nearly a third of the global population, and has the capacity to invade any nucleated cell in warm-blooded animals. Its parasitic success lies in its capacity to induce chronic infections while both avoiding immune detection and altering host immune responses and drug resistance. Toxoplasma infection can be acquired if a host becomes immunocompromised, such as during pregnancy, HIV/AIDS infection, or cancer. Infection with toxoplasmosis can be fatal during pregnancy if not treated on time; during the first trimester, it can cause serious complications like miscarriage or stillbirth, and during late pregnancy, the parasite can be transmitted to the developing fetus and cause severe complications like blindness, seizures, and hearing loss in the newborn.

Current treatments are limited and mostly ineffective against tissue cysts, and there is limited information on host immune modulation by T. gondii effectors. A T. gondii cyst remains dormant inside the host unless it is activated by a lack of functional immune response or an immunocompromised condition like pregnancy. Exosome-based studies have recently emerged regarding the pathogenicity and treatment of toxoplasmosis.

This Special Issue aims to uncover the latest drug targets identified for treating T. gondii, which can include exosome-based drugs, or nanoparticle-based or plant-extract-based therapies, with known mechanisms of targeting chronic infections or alleviating immunocompromised conditions. This article will also present the latest research on host–parasite interactions; the role of virulent invasive proteins in helping T. gondii cross the placental barrier during congenital infection; the role of effector molecules in the immune response; and newly identified proteins secreted by the parasite, which may play a significant role in its biology or pathogenesis.

Dr. Namrata Anand
Guest Editor

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Keywords

  • T. gondii
  • treatment strategies
  • secretory proteins
  • immune response
  • exosomes
  • nanoparticle
  • congenital infection
  • host–parasite interaction

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Published Papers (1 paper)

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Research

12 pages, 1225 KB  
Article
Differential Modulation of Hepatic Akt/mTOR Signaling During Acute and Chronic Toxoplasma gondii Infection in a Murine Model
by Jianchun Xiao
Cells 2026, 15(10), 893; https://doi.org/10.3390/cells15100893 (registering DOI) - 14 May 2026
Abstract
Toxoplasma gondii is an obligate intracellular parasite that infects virtually all warm-blooded animals, progressing through acute and chronic stages. The Akt/mTOR signaling axis plays critical roles in cell survival, proliferation, and metabolism, making it a key target for intracellular pathogens. This study investigated [...] Read more.
Toxoplasma gondii is an obligate intracellular parasite that infects virtually all warm-blooded animals, progressing through acute and chronic stages. The Akt/mTOR signaling axis plays critical roles in cell survival, proliferation, and metabolism, making it a key target for intracellular pathogens. This study investigated how T. gondii infection modulates this pathway during both infections. Outbred CD-1 mice were infected intraperitoneally with the virulent GT1 strain of T. gondii. Mice for acute studies were sacrificed five days post-infection, while those for chronic studies were treated with sulfadiazine and sacrificed five months post-infection. Phosphoprotein expression of eight Akt/mTOR pathway components was measured in liver tissues using a multiplexed bead-based immunoassay. Acute T. gondii infection caused broad suppression of Akt/mTOR signaling, with 6 of 8 markers significantly downregulated, including pS6RPSer235/236, pAKTS473, pBADSer136, pIRS1S636/639, pPTENSer380, and pGSK-3α/βSer21/9. In contrast, chronic infection related to cyst burden selectively activates specific nodes of the pathway, including pBADSer136, pmTORSer2448, and pGSK-3α/βSer21/9. Infection induced strong correlations between inter-components, which reflect coherent and coordinated pathway-level reprogramming rather than random perturbation. These findings show that acute and chronic T. gondii infections have opposing effects on host Akt/mTOR signaling for their own benefit, which may present new therapeutic targets. Full article
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