Resistance to Experimental Visceral Leishmaniasis in Mice Infected With Leishmania infantum Requires Batf3.

Autor: Soto, 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
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Zdroj: Frontiers in Immunology; 12/10/2020, Vol. 11, pN.PAG-N.PAG, 10p
Abstrakt: 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. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index