@article{1366,
  keywords = {Cytokines, Dose-Response Relationship, Drug, Humans, Interferon-gamma, Interleukin-12, Interleukin-18, Killer Cells, Natural, leprosy, Monocytes, T-Lymphocytes, Tuberculosis, Pulmonary},
  author = {García V E and Uyemura K and Sieling P A and Ochoa M T and Morita C T and Okamura H and Kurimoto M and Rea T H and Modlin R L},
  title = {IL-18 promotes type 1 cytokine production from NK cells and T cells in human intracellular infection.},
  abstract = {<p>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-gamma 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-gamma 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-gamma production rapidly (24 h) by NK cells and in a more sustained manner (5 days) by T cells. Finally, IL-18 directly induced IFN-gamma 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.</p>},
  year = {1999},
  journal = {Journal of immunology (Baltimore, Md. : 1950)},
  volume = {162},
  pages = {6114-21},
  month = {1999 May 15},
  issn = {0022-1767},
  url = {http://www.jimmunol.org/content/162/10/6114.full.pdf+html},
  language = {eng},
}