title: Exacerbation of experimental autoimmune encephalomyelitis in mice deficient for DCIR, an inhibitory C-type lectin receptor.
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.
authors.forename: Akimasa
authors.initials: A
authors.lastname: Seno
authors.forename: Takumi
authors.initials: T
authors.lastname: Maruhashi
authors.forename: Tomonori
authors.initials: T
authors.lastname: Kaifu
authors.forename: Rikio
authors.initials: R
authors.lastname: Yabe
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Fujikado
authors.forename: Guangyu
authors.initials: G
authors.lastname: Ma
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Ikarashi
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kakuta
authors.forename: Yoichiro
authors.initials: Y
authors.lastname: Iwakura
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology / Q000473:pathology; D003711:Demyelinating Diseases / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology / Q000473:pathology; D018450:Disease Progression; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology*; D037181:Lectins, C-Type / Q000737:chemistry / Q000276:immunology*; D008198:Lymph Nodes / Q000276:immunology / Q000473:pathology; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009103:Multiple Sclerosis / Q000276:immunology*; D011971:Receptors, Immunologic / Q000737:chemistry / Q000276:immunology*; D015398:Signal Transduction / Q000276:immunology*; D013116:Spinal Cord / Q000276:immunology / Q000473:pathology
chemical_list: D037181:Lectins, C-Type; D011971:Receptors, Immunologic; C477518:dendritic cell immunoactivating receptor, mouse