title: Expression and functional characterization of retinoic acid-inducible gene-I-like receptors of mast cells in response to viral infection.
abstract: To investigate the precise mechanisms of virus recognition by mast cells, the expression and functional characteristics of virus recognition receptors that lead to mast cell activation were investigated. Our results suggest that mast cells are partly responsible for the early in vivo production of antiviral cytokines and chemokines upon vesicular stomatitis virus (VSV) infection. Analysis of the expression of double-stranded RNA (dsRNA) recognition receptors in murine bone marrow-derived mast cells (BMMCs) revealed that BMMCs express melanoma differentiation-associated gene 5 (MDA5), protein kinase RNA-activated, retinoic acid-inducible gene-I (RIG-I) and Toll-like receptor 3. The expression levels of these receptors were found to increase upon stimulation of mast cells with VSV as well as synthetic dsRNA: polyinosinic-polycytidylic acid. Moreover, small interfering RNA analysis to identify the receptors responsible for mast cell activation by VSV revealed that both RIG-I and MDA5 were involved in cytokine production but not in the degranulation of mast cells. Our findings suggest that mast cells produce cytokines and chemokines in the early infection stage after recognizing viruses via RIG-I and MDA5, and may contribute to antiviral responses. These data provide additional novel information that improves our understanding of antiviral innate responses that involve mast cells.
authors.affiliation: Department of Infection Control Science, Juntendo University School of Medicine, Tokyo, Japan.
authors.forename: Minoru
authors.initials: M
authors.lastname: Fukuda
authors.forename: Hiroko
authors.initials: H
authors.lastname: Ushio
authors.forename: Junko
authors.initials: J
authors.lastname: Kawasaki
authors.forename: Francois
authors.initials: F
authors.lastname: Niyonsaba
authors.forename: Mizuho
authors.initials: M
authors.lastname: Takeuchi
authors.forename: Tadashi
authors.initials: T
authors.lastname: Baba
authors.forename: Keiichi
authors.initials: K
authors.lastname: Hiramatsu
authors.forename: Ko
authors.initials: K
authors.lastname: Okumura
authors.forename: Hideoki
authors.initials: H
authors.lastname: Ogawa
mesh_terms: D000818:Animals; D001853:Bone Marrow / Q000276:immunology; D015550:Cell Degranulation / Q000235:genetics / Q000276:immunology; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism; D053487:DEAD-box RNA Helicases / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation; D007113:Immunity, Innate / Q000235:genetics; D000072640:Interferon-Induced Helicase, IFIH1; D008407:Mast Cells / Q000276:immunology* / Q000821:virology; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000235:genetics; D012367:RNA, Viral / Q000276:immunology; D011956:Receptors, Cell Surface; D051196:Toll-Like Receptor 3 / Q000235:genetics / Q000378:metabolism; D054243:Vesicular Stomatitis / Q000276:immunology*; D018116:Vesiculovirus / Q000276:immunology*; D000097905:Roundabout Proteins
chemical_list: D016207:Cytokines; D053487:DEAD-box RNA Helicases; D000072640:Interferon-Induced Helicase, IFIH1; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; D034741:RNA, Small Interfering; D012367:RNA, Viral; D011956:Receptors, Cell Surface; D051196:Toll-Like Receptor 3; C118348:Robo3 protein, mouse; D000097905:Roundabout Proteins; C510592:Ifih1 protein, mouse