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*
Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115; and
Department of Host Defense, Osaka University, Osaka, Japan
IL-18 has been shown to play a critical role in the development of
a Th1 response and immunity against intracellular pathogens. To
determine the role of IL-18 in the development of protective immunity
against Leishmania major, we have analyzed the course of
cutaneous L. major in IL-18-deficient C57BL/6 mice
(IL-18-/-) compared with similarly infected wild-type
mice (IL-18+/+). After L. major infection,
IL-18-/- mice may develop larger lesions during early
phase of infection but eventually will resolve them as efficiently as
IL-18+/+ mice. By 2 wk after infection, although
Ag-stimulated lymph node cells from L. major-infected
IL-18+/+ and IL-18-/- mice produced similar
levels of IFN-
, those from IL-18-/- mice produced
significantly more IL-12 and IL-4. By 10 wk after infection, both
IL-18+/+ and IL-18-/- mice had resolved
L. major infection. At this time, lymph node cells from
both IL-18+/+ and IL-18-/- mice produced
IL-12 and IFN- but no IL-4. Furthermore, administration of
anti-IFN- Abs to IL-18-/- mice rendered them
susceptible to L. major. These results indicate that
despite the role IL-18 may play in early control of cutaneous L.
major lesion growth, this cytokine is not critical for
development of protective Th1 response and resolution of L.
major infection.
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