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

Research output: Contribution to journalArticlepeer-review

26 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)109-119
Number of pages11
JournalExperimental Animals
Issue number2
Publication statusPublished - 2015
Externally publishedYes


  • C-type lectin receptor
  • Dendritic cell immunoreceptor
  • Experimental autoimmune encephalomyelitis
  • Multiple sclerosis

ASJC Scopus subject areas

  • Animal Science and Zoology
  • Biochemistry, Genetics and Molecular Biology(all)
  • veterinary(all)


Dive into the research topics of 'Exacerbation of experimental autoimmune encephalomyelitis in mice deficient for DCIR, an inhibitory C-type lectin receptor'. Together they form a unique fingerprint.

Cite this