title: IgE- and FcepsilonRI-mediated enhancement of surface CD69 expression in basophils: role of low-level stimulation.
abstract: Surface-expressed CD69 is a recently recognized activation marker for basophils and is reported to be strongly induced in vitro by IL-3. In this study, we investigated whether IgE- and high-affinity receptor for IgE (FcepsilonRI)-dependent stimuli can affect basophil CD69 expression. Highly purified basophils were cultured for 24 h in the presence of anti-FcepsilonRI alpha-chain mAb, CRA-1 and IL-3, and surface CD69 expression was analyzed by flow cytometry. CRA-1 mAb at 1 ng/ml or lower concentrations, levels too low to provoke direct histamine release, dose-dependently enhanced surface CD69 expression in the presence of IL-3, although low-dose CRA-1 mAb failed to induce CD69 expression in the absence of IL-3. Recombinant Der f 2 at 10 to 100 pg/ml enhanced CD69 levels in the presence of IL-3 in basophils from mite-sensitive subjects. These results suggest that allergens may influence basophil CD69 expression even when the levels of the antigens are too low to trigger direct degranulation. Upregulated CD69 expression on locally accumulated basophils in bronchial asthma may be attributed at least in part to a combination of local cytokines, especially IL-3, plus exposure to low levels of IgE-crosslinking allergens.
authors.affiliation: Department of Allergy and Rheumatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
authors.forename: Maho
authors.initials: M
authors.lastname: Suzukawa
authors.forename: Akiko
authors.initials: A
authors.lastname: Komiya
authors.forename: Chitose
authors.initials: C
authors.lastname: Yoshimura-Uchiyama
authors.forename: Ayako
authors.initials: A
authors.lastname: Kawakami
authors.forename: Rikiya
authors.initials: R
authors.lastname: Koketsu
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Nagase
authors.forename: Motoyasu
authors.initials: M
authors.lastname: Iikura
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Yamada
authors.forename: Chisei
authors.initials: C
authors.lastname: Ra
authors.forename: Ken
authors.initials: K
authors.lastname: Ohta
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Masao
authors.initials: M
authors.lastname: Yamaguchi
mesh_terms: D000485:Allergens / Q000276:immunology*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology; D015703:Antigens, CD / Q000096:biosynthesis* / Q000235:genetics; D039741:Antigens, Dermatophagoides / Q000276:immunology*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis* / Q000235:genetics; D060829:Arthropod Proteins; D001249:Asthma / Q000209:etiology / Q000276:immunology*; D001491:Basophils / Q000276:immunology* / Q000378:metabolism; D002478:Cells, Cultured / Q000276:immunology; D016207:Cytokines / Q000502:physiology; D004306:Dose-Response Relationship, Immunologic; D006636:Histamine Release / Q000276:immunology; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology; D007377:Interleukin-3 / Q000276:immunology*; D037181:Lectins, C-Type; D051379:Mice; D039981:Pyroglyphidae / Q000276:immunology; D017455:Receptors, IgE / Q000037:antagonists & inhibitors / Q000276:immunology*; D015854:Up-Regulation / Q000276:immunology; D000099192:CD69 Antigens
chemical_list: D000485:Allergens; D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D039741:Antigens, Dermatophagoides; D000945:Antigens, Differentiation, T-Lymphocyte; D060829:Arthropod Proteins; D016207:Cytokines; D007073:Immunoglobulin E; D007074:Immunoglobulin G; D007377:Interleukin-3; D037181:Lectins, C-Type; D017455:Receptors, IgE; D000099192:CD69 Antigens; C451160:Dermatophagoides farinae antigen f 2; C475664:FCER1A protein, human; C508596:IL3 protein, human