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*
Division of Dermatology and
Department of Microbiology and Immunology, University of California, Los Angeles, School of Medicine, Los Angeles, CA 90095;
Division of Rheumatology and Immunology, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115;
§
Hyogo College of Medicine, Mukogawa-cho, Nishinomiya, Japan;
¶
Fujisaki Institute, Hayashibara Biochemical Labs, Fujisaki, Okayama, Japan; and
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Section of Dermatology, University of Southern California School of Medicine, Los Angeles, CA 90033
We investigated the role of IL-18 in leprosy, a disease
characterized by polar cytokine responses that correlate with clinical
disease. In vivo, IL-18 mRNA expression was higher in lesions from
resistant tuberculoid as compared with susceptible lepromatous
patients, and, in vitro, monocytes produced IL-18 in response to
Mycobacterium leprae. rIL-18 augmented M.
leprae-induced IFN-
in tuberculoid patients, but not
lepromatous patients, while IL-4 production was not induced by IL-18.
Anti-IL-12 partially inhibited M. leprae-induced release
of IFN- in the presence of IL-18, suggesting a combined effect of
IL-12 and IL-18 in promoting M. leprae-specific type 1
responses. IL-18 enhanced M. leprae-induced IFN-
production rapidly (24 h) by NK cells and in a more sustained manner (5
days) by T cells. Finally, IL-18 directly induced IFN- production
from mycobacteria-reactive T cell clones. These results suggest that
IL-18 induces type 1 cytokine responses in the host defense against
intracellular infection.
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