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Monocytes/macrophages infected with Toxoplasma gondii do not increase co-stimulatory molecules while maintaining their migratory ability

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Abstract:

Seipel D, Ribeiro-Gomes FL, Barcelos MW, Ramalho AV, Kanashiro MM, Kipnis TL, Arnholdt ACV. Monocytes/macrophages infected with Toxoplasma gondii do not increase co-stimulatory molecules while maintaining their migratory ability. APMIS 2009; 117: 672–80.

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 ofl-selectin and β2 integrin was unaltered. We evaluated the ability of infected macrophages from wild type C57/BL/6 or CD14−/− mice to migrate in 8 μm 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.

Keywords: CD80; T. gondii; l-selectin; migration; β2 integrin

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1600-0463.2009.02519.x

Affiliations: 1: Laboratório de Biologia do Reconhecer, Centro de Biociências e Biotecnologia, Universidade Estadual do Norte Fluminense 2: Hospital Geral de Guarus, PMCG; Campos dos Goytacazes, Rio de Janeiro, Brazil

Publication date: September 1, 2009

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