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Essential Role of CD8⁺CD122⁺ Regulatory T Cells in the Recovery from Experimental Autoimmune Encephalomyelitis¹

Young-Ho Lee^*, Yoshiyuki Ishida, Muhaimin Rifa’i^*,,, Zhe Shi^*, Ken-ichi Isobe^* and Haruhiko Suzuki^2,*

^* Department of Immunology, Nagoya University Graduate School of Medicine, Radioisotope Research Center, Medical Branch of Nagoya University, Nagoya, and Japan Society for the Promotion of Science, Tokyo, Japan; and Brawijaya University, East-Java, Indonesia

Experimental autoimmune encephalomyelitis (EAE) is one of the best-documented animal models of autoimmune disease. We examined the role of CD8⁺CD122⁺ regulatory T cells, which we previously identified as naturally occurring regulatory T cells that effectively regulate CD8⁺ T cells, in EAE. Depletion of CD8⁺CD122⁺ regulatory T cells by in vivo administration of anti-CD122 mAb resulted in persistent EAE symptoms. Transfer of CD8⁺CD122⁺ regulatory T cells into EAE mice at the peak EAE score clearly improved symptoms, indicating an important role of CD8⁺CD122⁺ regulatory T cells in the recovery phase of EAE. This was further confirmed by an increase and a decrease in the number of infiltrating T cells in the CNS and T cell cytokine production in mice that were depleted of or complemented with CD8⁺CD122⁺ cells. Furthermore, transfer of preactivated CD8⁺CD122⁺ regulatory T cells resulted in diminished EAE symptoms, especially in the recovery phase of EAE. These results elucidate the essential role of CD8⁺CD122⁺ regulatory T cells in the recovery phase of EAE and suggest the preventive effect of preactivated CD8⁺CD122⁺ regulatory T cells for EAE.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan and from the Japan Society for the Promotion of Science.

² Address correspondence and reprint requests to Dr. Haruhiko Suzuki, Department of Immunology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan. E-mail address: k46200a{at}nucc.cc.nagoya-u.ac.jp

³ Abbreviations used in this paper: EAE, experimental autoimmune encephalomyelitis; MOG, myelin oligodendrocyte glycoprotein; MS, multiple sclerosis; MBP, myelin basic protein; nTreg, naturally occurring regulatory T cell; EGFP, enhanced GFP; PLP, proteolipid protein.

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