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by NK Cells1
*
Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden;
Department of Immunology, The Scripps Research Institute, La Jolla, CA 92037;
Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Osaka University, Osaka, Japan
IL-18 promotes NK cell and Th1 cell activity and may bridge innate
and adaptive immune responses. Myelin oligodendrocyte glycoprotein
(MOG) is a myelin component of the CNS and is a candidate autoantigen
in multiple sclerosis. In the present study we show that
IL-18-deficient (IL-18-/-) mice are defective in mounting
autoreactive Th1 and autoantibody responses and are resistant to
MOG35–55 peptide-induced autoimmune encephalomyelitis.
IL-18 administration enhances the disease severity in wild-type mice
and restores the ability to generate Th1 response in the
IL-18-/- mice. This restoration was abrogated in NK
cell-depleted mice, indicating that the action of IL-18 in promoting
the generation of MOG-specific Th cells was dependent on NK cells.
Furthermore, transfer of NK cells from recombinase-activating gene
1-/- mice, but not from recombinase-activating gene
1/IFN-
-/- mice, rescued the defective Th1 responses in
IL-18-/- mice and rendered IL-18-/- mice
susceptible to the induction of autoimmune encephalomyelitis. Thus,
IL-18 can direct autoreactive T cells and promote autodestruction in
the CNS at least in part via induction of IFN- by NK
cells.
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