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

• DOI: 10.1538/expanim.14-0079
• Publication Date: 2014-12-14T23:17:16Z
• Authors: Akimasa SENO; Takumi MARUHASHI; Tomonori KAIFU; Rikio YABE; Noriyuki FUJIKADO; Guangyu MA; Tetsuro IKARASHI; Shigeru KAKUTA; Yoichiro IWAKURA
• Keywords: Myelin oligodendrocyte glycoprotein; Encephalomyelitis; C-type lectin; CD11c

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