Exacerbation of experimental autoimmune encephalomyelitis in mice deficient          for DCIR, an inhibitory C-type lectin receptor

Akimasa SENO; Takumi MARUHASHI; Tomonori KAIFU; Rikio YABE; Noriyuki FUJIKADO; Guangyu MA; Tetsuro IKARASHI; Shigeru KAKUTA; Yoichiro IWAKURA

doi:10.1538/expanim.14-0079

Originals

Exacerbation of experimental autoimmune encephalomyelitis in mice deficient for DCIR, an inhibitory C-type lectin receptor

Akimasa SENO, Takumi MARUHASHI, Tomonori KAIFU, Rikio YABE, Noriyuki FUJIKADO, Guangyu MA, Tetsuro IKARASHI, Shigeru KAKUTA, Yoichiro IWAKURA

Author information

Akimasa SENO
Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda-shi, Chiba 278-0022, Japan
Department of Computational Biology, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa-shi, Chiba 277-0882, Japan
Takumi MARUHASHI
Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda-shi, Chiba 278-0022, Japan
Tomonori KAIFU
Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda-shi, Chiba 278-0022, Japan
Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi-shi, Saitama 332-0012, Japan
Rikio YABE
Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda-shi, Chiba 278-0022, Japan
Noriyuki FUJIKADO
Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
Guangyu MA
Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
Tetsuro IKARASHI
Department of Biomedical Science, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
Shigeru KAKUTA
Department of Biomedical Science, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
Yoichiro IWAKURA
Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan
Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda-shi, Chiba 278-0022, Japan
Department of Computational Biology, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa-shi, Chiba 277-0882, Japan
Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Kawaguchi-shi, Saitama 332-0012, Japan
Medical Mycology Research Center, Chiba University, Chuo-ku, Chiba 250-8673, Japan

Keywords: C-type lectin receptor, dendritic cell immunoreceptor, experimental autoimmune encephalomyelitis, multiple sclerosis

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Supplementary material

2015 Volume 64 Issue 2 Pages 109-119

DOI https://doi.org/10.1538/expanim.14-0079

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Abstract

Dendritic cell immunoreceptor (DCIR) is a C-type lectin receptor containing a carbohydrate recognition domain in its extracellular portion and an immunoreceptor tyrosine–based inhibitory motif, which transduces negative signals into cells, in its cytoplasmic portion. Previously, we showed that Dcir^–/– mice spontaneously develop autoimmune diseases such as enthesitis and sialadenitis due to excess expansion of dendritic cells (DCs), suggesting that DCIR is critically important for the homeostasis of the immune system. In this report, we analyzed the role of DCIR in the development of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model for multiple sclerosis. We found that EAE was exacerbated in Dcir^–/– mice associated with severe demyelination of the spinal cords. The number of infiltrated CD11c⁺ DCs and CD4⁺ T cells into spinal cords was increased in Dcir^–/– mice. Recall proliferative response of lymph node cells was higher in Dcir^–/– mice compared with wild-type mice. These observations suggest that DCIR is an important negative regulator of the immune system, and Dcir^–/– mice should be useful for analyzing the roles of DCIR in an array of autoimmune diseases.

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