The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/11/1677/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 10, November 17, 1997 1677-1687

Articles

Regulation of Experimental Autoimmune Encephalomyelitis by Natural Killer (NK) Cells

Ben-ning Zhang*,{ddagger}, Takashi Yamamura*, Takayuki Kondo*, Michio Fujiwara{ddagger}, and Takeshi Tabira*

From the * Department of Demyelinating Disease and Aging, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo 187, Japan; and {ddagger} Animal Center for Biomedical Research, Faculty of Medicine, The University of Tokyo, Bunkyo-ku, Tokyo 113, Japan

In this report, we establish a regulatory role of natural killer (NK) cells in experimental autoimmune encephalomyelitis (EAE), a prototype T helper cell type 1 (Th1)-mediated disease. Active sensitization of C57BL/6 (B6) mice with the myelin oligodendrocyte glycoprotein (MOG)35-55 peptide induces a mild form of monophasic EAE. When mice were deprived of NK cells by antibody treatment before immunization, they developed a more serious form of EAE associated with relapse. Aggravation of EAE by NK cell deletion was also seen in β2-microglobulin–/– (β2m–/–) mice, indicating that NK cells can play a regulatory role in a manner independent of CD8+ T cells or NK1.1+ T cells (NK–T cells). The disease enhancement was associated with augmentation of T cell proliferation and production of Th1 cytokines in response to MOG35-55. EAE passively induced by the MOG35-55-specific T cell line was also enhanced by NK cell deletion in B6, β2m–/–, and recombination activation gene 2 (RAG-2)–/– mice, indicating that the regulation by NK cells can be independent of T, B, or NK–T cells. We further showed that NK cells inhibit T cell proliferation triggered by antigen or cytokine stimulation. Taken together, we conclude that NK cells are an important regulator for EAE in both induction and effector phases.

Address correspondence to Takashi Yamamura, Department of Demyelinating Disease and Aging, National Institute of Neuroscience, NCNP, 4-1-1 Ogawahigashi, Kodaira, Tokyo 187, Japan. FAX: +81-423-46-1747; Phone: +81-423-41-2711; E-mail: yamamura{at}ncnaxp.ncnp.go.jp

1 Abbreviations used in this paper: β2m; β2-microglobulin; EAE, experimental autoimmune encephalomyelitis; MOG, myelin oligodendrocyte glycoprotein; PT, pertussis toxin; RAG, recombination activation gene.


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