| First Author | Soto M | Year | 2020 |
| Journal | Front Immunol | Volume | 11 |
| Pages | 590934 | PubMed ID | 33362772 |
| Mgi Jnum | J:311681 | Mgi Id | MGI:6728930 |
| Doi | 10.3389/fimmu.2020.590934 | Citation | Soto M, et al. (2020) Resistance to Experimental Visceral Leishmaniasis in Mice Infected With Leishmania infantum Requires Batf3. Front Immunol 11:590934 |
| abstractText | 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-gamma production. Our results reinforce the implication of Batf3 in the generation of type 1 immunity against infectious diseases. |
