IL-12 gene-deficient C57BL / 6 mice are susceptible toLeishmania donovani but have diminished hepatic immunopathology

This is the authors' abstract. We don't add key points for this paper.

To determine the in vivo role of IL-12 in the development of protective immunity in visceral leishmaniasis caused by Leishmania donovani, we examined the course of L. donovani infection in IL-12-deficient C57BL/6 (IL-12-/-) mice. IL-12-/- mice displayed significantly higher parasite burdens in their livers and spleens than wild-type C57BL/6 mice throughout the course of infection. Despite high parasite burdens, the onset of hepatosplenomegaly was significantly delayed in L. donovani-infected IL-12-/-. Moreover, livers and spleens from IL-12-/- mice displayed significantly less inflammation and poorly formed granulomatous lesions than those from IL-12+/+ mice throughout the course of infection. Antigen-stimulated splenocytes from IL-12-/- mice produced significantly less IFN-gamma but more IL-4 than IL-12+/+ mice. These findings indicate that although endogenous IL-12 is critical for the development of protective immunity to L. donovani, it is also responsible for inducing the significant immunopathology associated with visceral leishmaniasis.