Gutcher I Urich E Wolter K Prinz M Becher B 2006 T helper type 1 (T(H)1) 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 T(H)1 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 alpha-deficient mice were resistant to experimental autoimmune encephalomyelitis, indicating involvement of an IL-18R alpha ligand other than IL-18 with encephalitogenic properties. Moreover, engagement of IL-18R alpha on antigen-presenting cells was required for the generation of pathogenic IL-17-producing T helper cells. Thus, IL-18 and T(H)1 cells are dispensable, whereas IL-18R alpha and IL-17-producing T helper cells are required, for autoimmune central nervous system inflammation. application/pdf https://sonar.ch/global/documents/75247 eng info:eu-repo/semantics/altIdentifier/doi/10.1038/ni1377 info:eu-repo/semantics/altIdentifier/pmid/16906165 info:eu-repo/semantics/openAccess Nature immunology. - 2006 Animals Antigen-Presenting Cells Antigens Encephalomyelitis, Autoimmune, Experimental Interleukin-12 Interleukin-17 Interleukin-18 Interleukin-23 Mice Mice, Knockout Mitogens Receptors, Interleukin-18 Th1 Cells Interleukin 18-independent engagement of interleukin 18 receptor-alpha is required for autoimmune inflammation. http://purl.org/coar/resource_type/c_6501