First Author | Satoskar AR | Year | 2000 |
Journal | Eur J Immunol | Volume | 30 |
Issue | 3 | Pages | 834-9 |
PubMed ID | 10741399 | Mgi Jnum | J:60891 |
Mgi Id | MGI:1354059 | Doi | 10.1002/1521-4141(200003)30:3<834::AID-IMMU834>3.0.CO;2-9 |
Citation | Satoskar AR, et al. (2000) IL-12 gene-deficient C57BL/6 mice are susceptible to Leishmania donovani but have diminished hepatic immunopathology. Eur J Immunol 30(3):834-9 |
abstractText | 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. |