title: Basophils play a critical role in the development of IgE-mediated chronic allergic inflammation independently of T cells and mast cells.
abstract: The recruitment of basophils into the sites of allergic inflammation is often observed. However, no definitive evidence has been provided that basophils are crucially involved in the pathogenesis of chronic allergic disorders. Here, we show that basophils are responsible for the development of IgE-mediated chronic allergic inflammation independently of T cells and mast cells. A single subcutaneous injection of multivalent antigens elicited not only immediate- and late-phase ear swelling but also delayed-onset ear swelling with massive eosinophil infiltration in mice sensitized with antigen-specific IgE. Mast cells were essential for the immediate- and late-phase ear swelling but dispensable for the delayed one. T cells were also dispensable for the latter. Transfer of FcRI-expressing basophils into FcRI-deficient mice restored the development of the delayed-onset allergic inflammation. These findings indicate a novel mechanism of development of chronic allergic inflammation that is induced by basophils through the interaction of antigen, IgE, and FcRI.
authors.affiliation: Department of Immune Regulation, Tokyo Medical and Dental University Graduate School, Bunkyo-ku, Japan.
authors.forename: Kaori
authors.initials: K
authors.lastname: Mukai
authors.forename: Kunie
authors.initials: K
authors.lastname: Matsuoka
authors.forename: Choji
authors.initials: C
authors.lastname: Taya
authors.forename: Hidenori
authors.initials: H
authors.lastname: Suzuki
authors.forename: Hiroo
authors.initials: H
authors.lastname: Yokozeki
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Nishioka
authors.forename: Katsuiku
authors.initials: K
authors.lastname: Hirokawa
authors.forename: Maki
authors.initials: M
authors.lastname: Etori
authors.forename: Makoto
authors.initials: M
authors.lastname: Yamashita
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Kubota
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Minegishi
authors.forename: Hiromichi
authors.initials: H
authors.lastname: Yonekawa
authors.forename: Hajime
authors.initials: H
authors.lastname: Karasuyama
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D001491:Basophils / Q000276:immunology*; D002908:Chronic Disease; D006967:Hypersensitivity / Q000276:immunology* / Q000378:metabolism / Q000473:pathology*; D007073:Immunoglobulin E / Q000502:physiology*; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D007694:Killer Cells, Natural / Q000276:immunology; D008407:Mast Cells / Q000276:immunology*; D051379:Mice; D008805:Mice, Inbred A; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D018345:Mice, Knockout; D017455:Receptors, IgE / Q000502:physiology*; D012867:Skin / Q000378:metabolism / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D017455:Receptors, IgE; D015847:Interleukin-4; D007073:Immunoglobulin E