Resistance to experimental visceral leishmaniasis in mice infected with leishmania infantum requires Batf3

Unveiling the protective immune response to visceral leishmaniasis is critical for a rational design of vaccines aimed at reducing the impact caused by this fatal, if left untreated, vector-borne disease. In this study we sought to determine the role of the basic leucine zipper transcription factor...

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Detalles Bibliográficos
Autores: Soto Álvarez, Manuel, Ramírez, Laura, Solana, José Carlos, Cook, Emma C.L., Hernández-García, Elena, Charro-Zanca, Sara, Redondo-Urzainqui, Ana, Reguera, Rosa M., Balaña-Fouce, Rafael, Iborra, Salvador
Tipo de recurso: artículo
Fecha de publicación:2020
País:España
Institución:Universidad Autónoma de Madrid
Repositorio:Biblos-e Archivo. Repositorio Institucional de la UAM
Idioma:inglés
OAI Identifier:oai:repositorio.uam.es:10486/711238
Acceso en línea:http://hdl.handle.net/10486/711238
https://dx.doi.org/10.3389/fimmu.2020.590934
Access Level:acceso abierto
Palabra clave:Batf3
Batf3 DC+
Leishmania
Th1 responses
Visceral leishmaniasis
Dendritic cells
Biología y Biomedicina / Biología
Descripción
Sumario:Unveiling the protective immune response to visceral leishmaniasis is critical for a rational design of vaccines aimed at reducing the impact caused by this fatal, if left untreated, vector-borne disease. In this study we sought to determine the role of the basic leucine zipper transcription factor ATF-like 3 (Batf3) in the evolution of infection with Leishmania infantum, the causative agent of human visceral leishmaniasis in the Mediterranean Basin and Latin America. For that, Batf3-deficient mice in C57BL/6 background were infected with an L. infantum strain expressing the luciferase gene. Bioluminescent imaging, as well as in vitro parasite titration, demonstrated that Batf3-deficient mice were unable to control hepatic parasitosis as opposed to wild-type C57BL/6 mice. The impaired microbicide capacities of L. infantum-infected macrophages from Batf3-deficient mice mainly correlated with a reduction of parasite-specific IFN-γ production. Our results reinforce the implication of Batf3 in the generation of type 1 immunity against infectious diseases