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Updated: Jun 20, 2026
Forward Genetics Screens Using Macrophages to Identify Toxoplasma gondii Genes Important for Resistance to IFN-γ-Dependent Cell Autonomous Immunity
Published on: March 12, 2015
Monocytes/macrophages infected with Toxoplasma gondii do not increase co-stimulatory molecules while maintaining
Daniele Seipel1, Flavia Lima Ribeiro-Gomes, Michelle Willmen Barcelos
1Laboratório de Biologia do Reconhecer, Centro de Biociências e Biotecnologia, Universidade Estadual do Norte Fluminense. Rio de Janeiro, Brazil.
Abstract:
Toxoplasma gondii is an obligate intracellular parasite that is able to disseminate into deep tissues and cross biological barriers, reaching immunoprivileged sites such as the brain and retina. The parasite is able to infect macrophages and dendritic cells and use them for dispersal throughout the body, but the activation state of those cells is unknown. We investigated the ability of human and murine cells from monocytic/macrophage lineages that had not previously been exposed to inflammatory cytokines to up-regulate co-stimulatory and adhesion molecules upon infection. Toxoplasma gondii-infected human monocytes (freshly isolated and THP1 lineage) were unable to up-regulate CD86, CD83, CD40 or CD1a. CD80 expression increased in infected cells but expression of l-selectin and beta2 integrin was unaltered. We evaluated the ability of infected macrophages from wild type C57/BL/6 or CD14(-/-) mice to migrate in 8 mum transwells. Infected cells from CD14(-/-) mice were more likely to de-adhere than infected cells from wild type mice but they did not show any increase in migratory ability. The non-stimulatory profile of these infected cells may contribute to parasite spread throughout the lymphatic circulation in the initial phases of infection.
Insights
Toxoplasma gondii infection does not activate immune cells like monocytes and macrophages, hindering their ability to stimulate an immune response. This lack of activation may facilitate parasite spread during the early stages of infection.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- Toxoplasma gondii is an intracellular parasite that disseminates to deep tissues and crosses biological barriers.
- Macrophages and dendritic cells are infected by T. gondii and aid its dispersal, but their activation state is unknown.
Purpose of the Study:
- To investigate the activation state of human and murine monocytic/macrophage lineage cells upon T. gondii infection.
- To determine if T. gondii infection alters the expression of co-stimulatory and adhesion molecules.
- To assess the migratory capacity of infected macrophages.
Main Methods:
- Infection of human monocytes (freshly isolated and THP1) and murine macrophages (wild type and CD14(-/-)) with T. gondii.
- Analysis of co-stimulatory molecules (CD86, CD83, CD40, CD1a, CD80) and adhesion molecules (l-selectin, beta2 integrin) expression.
- Transwell migration assays for infected murine macrophages.
Main Results:
- T. gondii-infected human monocytes showed no significant upregulation of CD86, CD83, CD40, or CD1a.
- CD80 expression increased in infected human cells, but l-selectin and beta2 integrin expression remained unaltered.
- Infected CD14(-/-) murine macrophages showed increased de-adhesion but no enhanced migration compared to wild-type.
Conclusions:
- T. gondii infection induces a non-stimulatory profile in monocytes and macrophages.
- This lack of immune cell activation may contribute to parasite dissemination via lymphatic circulation in early infection stages.
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