Responses to Leishmania donovani in Mice Deficient in Interleukin-12 (IL-12), IL-12/IL-23, or IL-18

Interleukin-12 (IL-12) orchestrates acquired resistance in intracellular Leishmania donovani infection in the liver, inducing gamma interferon and, in turn, macrophage activation and parasite killing. Nevertheless, testing in IL-18⁻/⁻ mice compared to wild-type mice and in IL-12p40⁻/⁻ compared to IL...

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Bibliographic Details
Published in:Infection and Immunity 2006-07, Vol.74 (7), p.4370-4374
Main Authors: Murray, Henry W, Tsai, Christine W, Liu, Jianguo, Ma, Xiaojing
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Female
Fundamental and applied biological sciences. Psychology
Fungal and Parasitic Infections
Genetic Predisposition to Disease
Immunity, Innate - genetics
Interferon-gamma - biosynthesis
Interleukin-12 - deficiency
Interleukin-12 - genetics
Interleukin-18 - deficiency
Interleukin-18 - genetics
Interleukin-23
Interleukin-23 Subunit p19
Interleukins - deficiency
Interleukins - genetics
Leishmania donovani
Leishmania donovani - immunology
Leishmaniasis, Visceral - genetics
Leishmaniasis, Visceral - immunology
Leishmaniasis, Visceral - metabolism
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Microbiology
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Summary:Interleukin-12 (IL-12) orchestrates acquired resistance in intracellular Leishmania donovani infection in the liver, inducing gamma interferon and, in turn, macrophage activation and parasite killing. Nevertheless, testing in IL-18⁻/⁻ mice compared to wild-type mice and in IL-12p40⁻/⁻ compared to IL-12p35⁻/⁻ mice also suggested both early-acting (IL-18) and late-acting (IL-23) antileishmanial effects independent of IL-12.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.00422-06