AUTHOR=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 

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

JOURNAL=Frontiers in Immunology

VOLUME=11

YEAR=2020

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2020.590934

DOI=10.3389/fimmu.2020.590934

ISSN=1664-3224

ABSTRACT=<p>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 <italic>Leishmania infantum</italic>, 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 <italic>L. infantum</italic> strain expressing the luciferase gene. Bioluminescent imaging, as well as <italic>in vitro</italic> 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 <italic>L. infantum</italic>-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.</p>