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

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Author(s)

    • SENO Akimasa SENO Akimasa
    • 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
    • MARUHASHI Takumi MARUHASHI Takumi
    • 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
    • KAIFU Tomonori [他] KAIFU Tomonori
    • 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
    • YABE Rikio
    • 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
    • FUJIKADO Noriyuki
    • 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
    • MA Guangyu
    • 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
    • IKARASHI Tetsuro
    • Department of Biomedical Science, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
    • KAKUTA Shigeru
    • Department of Biomedical Science, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan
    • IWAKURA Yoichiro
    • 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

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 <i>Dcir<sup>–/–</sup></i> 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 <i>Dcir<sup>–/–</sup></i> mice associated with severe demyelination of the spinal cords. The number of infiltrated CD11c<sup>+</sup> DCs and CD4<sup>+</sup> T cells into spinal cords was increased in <i>Dcir<sup>–/–</sup></i> mice. Recall proliferative response of lymph node cells was higher in <i>Dcir<sup>–/–</sup></i> mice compared with wild-type mice. These observations suggest that DCIR is an important negative regulator of the immune system, and <i>Dcir<sup>–/–</sup></i> mice should be useful for analyzing the roles of DCIR in an array of autoimmune diseases.

Journal

  • Experimental Animals

    Experimental Animals 64(2), 109-119, 2015

    Japanese Association for Laboratory Animal Science

Codes

  • NII Article ID (NAID)
    130005069862
  • NII NACSIS-CAT ID (NCID)
    AA11032321
  • Text Lang
    ENG
  • ISSN
    1341-1357
  • NDL Article ID
    026335791
  • NDL Call No.
    Z54-H752
  • Data Source
    NDL  J-STAGE 
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