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Journal article

Interleukin 18-independent engagement of interleukin 18 receptor-alpha is required for autoimmune inflammation.

  • 2006-08-15
Published in:
  • 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
English 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.
Language
  • English
Open access status
green
Identifiers
Persistent URL
https://sonar.ch/global/documents/75247
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