IL-12 gene-deficient C57BL / 6 mice are susceptible toLeishmania donovani but have diminished hepatic immunopathology
Copyright policy )IL-12 gene-deficient C57BL / 6 mice are susceptible toLeishmania donovani but have diminished hepatic immunopathology
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.
- Brigham and Women's Faulkner Hospital United States
- Beth Israel Deaconess Medical Center United States
- Harvard University United States
Male, Mice, Knockout, T-Lymphocytes, In Vitro Techniques, Lymphocyte Activation, Interleukin-12, Mice, Inbred C57BL, Interferon-gamma, Kinetics, Mice, Liver, Animals, Leishmaniasis, Visceral, Female, Interleukin-4, Spleen, Leishmania donovani
Male, Mice, Knockout, T-Lymphocytes, In Vitro Techniques, Lymphocyte Activation, Interleukin-12, Mice, Inbred C57BL, Interferon-gamma, Kinetics, Mice, Liver, Animals, Leishmaniasis, Visceral, Female, Interleukin-4, Spleen, Leishmania donovani
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