Nature Immunology
- 7, 946 - 953 (2006)
Published online: 13 August 2006; | doi:10.1038/ni1377
Interleukin 18–independent engagement of interleukin 18 receptor- is required for autoimmune inflammationIlona Gutcher1, Eduard Urich1, Karina Wolter2, Marco Prinz2 & Burkhard Becher11
Neuroimmunology Unit, Neurology Clinic, University of Zurich, 8057 Zurich, Switzerland
2
Institute of Neuropathology, Georg-August-University, D-37075 Gottingen, Germany.
Correspondence should be addressed to Burkhard Becher burkhard.becher@neuroimm.unizh.ch T helper type 1 (TH1) lymphocytes are considered to be the main pathogenic cell type responsible for organ-specific autoimmune inflammation. As interleukin 18 (IL-18) is a cofactor with IL-12 in promoting TH1 cell development, we examined the function of IL-18 and its receptor, IL-18R, in autoimmune central nervous system inflammation. Similar to IL-12-deficient mice, IL-18-deficient mice were susceptible to experimental autoimmune encephalomyelitis. In contrast, IL-18R -deficient mice were resistant to experimental autoimmune encephalomyelitis, indicating involvement of an IL-18R ligand other than IL-18 with encephalitogenic properties. Moreover, engagement of IL-18R on antigen-presenting cells was required for the generation of pathogenic IL-17-producing T helper cells. Thus, IL-18 and TH1 cells are dispensable, whereas IL-18R and IL-17-producing T helper cells are required, for autoimmune central nervous system inflammation.
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