title: Changing expression of IL-3 and IL-5 receptors in cultured human eosinophils.
abstract: IL-3, IL-5, and GM-CSF exert overlapping functions in eosinophils via a shared receptor beta-chain, and IL-3Ralpha transcript expression is the weakest in blood eosinophils. We investigated the long-term regulation of surface expression of IL-3Ralpha. IL-3 was the most potent inducer of CD69 expression after 24-h stimulation, but not after 1-h stimulation. Expression of IL-5Ralpha and GM-CSFRalpha was significantly downregulated by culturing with their respective ligands, while IL-3Ralpha expression was not. IL-3 at 30pM significantly increased IL-3Ralpha expression and IL-3Ralpha expression was also upregulated by both IL-5 and GM-CSF. In parallel with the surface protein expression, IL-3Ralpha mRNA was also upregulated by IL-3, IL-5, and GM-CSF. These results demonstrated that long-term culturing of eosinophils with CSFs induced a change in the potency order of CSFs, with IL-3 coming to exert the strongest effect. They thus suggest that IL-3 plays more important roles in local eosinophil activation than previously recognized.
authors.affiliation: Department of Allergy and Rheumatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
authors.forename: Chitose
authors.initials: C
authors.lastname: Yoshimura-Uchiyama
authors.forename: Masao
authors.initials: M
authors.lastname: Yamaguchi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Nagase
authors.forename: Kouji
authors.initials: K
authors.lastname: Matsushima
authors.forename: Takashi
authors.initials: T
authors.lastname: Igarashi
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Iwata
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Yamamoto
authors.forename: Koichi
authors.initials: K
authors.lastname: Hirai
mesh_terms: D015703:Antigens, CD / Q000096:biosynthesis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000096:biosynthesis; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D004804:Eosinophils / Q000378:metabolism*; D005434:Flow Cytometry; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D006684:HLA-DR Antigens / Q000096:biosynthesis; D006801:Humans; D007377:Interleukin-3 / Q000378:metabolism*; D015848:Interleukin-5 / Q000378:metabolism*; D007700:Kinetics; D037181:Lectins, C-Type; D008024:Ligands; D010957:Plasmids / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D016187:Receptors, Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D018123:Receptors, Interleukin / Q000096:biosynthesis*; D016185:Receptors, Interleukin-3 / Q000096:biosynthesis*; D053649:Receptors, Interleukin-5; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013997:Time Factors; D015854:Up-Regulation; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D006684:HLA-DR Antigens; D007377:Interleukin-3; D015848:Interleukin-5; D037181:Lectins, C-Type; D008024:Ligands; D012333:RNA, Messenger; D016187:Receptors, Granulocyte-Macrophage Colony-Stimulating Factor; D018123:Receptors, Interleukin; D016185:Receptors, Interleukin-3; D053649:Receptors, Interleukin-5; D000099192:CD69 Antigens