title: Activation markers of human basophils: CD69 expression is strongly and preferentially induced by IL-3.
abstract: BACKGROUND
  The biological functions of basophils are precisely regulated by various cytokines in vitro, but little is known about surface markers that are upregulated during the cytokine-mediated activation process.
  
  
  OBJECTIVE
  It has been well established that CD69, CD44, and CD54 represent "activation markers" for cytokine-mediated eosinophil activation. The objective of this study was to elucidate the expression and regulation of these molecules in human basophils in vitro as well as in vivo.
  
  
  METHODS
  Basophils were purified from venous blood by means of density gradient centrifugation followed by negative selection. Surface expression was analyzed by means of flow cytometry. We also studied the expression of CD69, CD44, and CD54 on basophils in bronchoalveolar lavage fluid and blood specimens from patients with asthma.
  
  
  RESULTS
  CD44 and CD54 were constitutively expressed on basophils and moderately upregulated by IL-3. On the other hand, CD69 expression was only weakly observed in freshly isolated basophils, but IL-3 induced extremely high levels of expression. Surface CD69 appeared rather slowly in comparison with CD63 and CD11b, and the induction of expression was completed within 24 hours. Basophil CD69 had no functional relevance, but it did have biological relevance. Whole blood basophils from asthmatic individuals expressed significantly higher levels of CD69 than did those from normal individuals. Furthermore, bronchoalveolar lavage fluid basophils showed higher levels of CD69 expression than did blood basophils from the same donors.
  
  
  CONCLUSIONS
  CD69 expression on basophils was preferentially and strongly upregulated by IL-3. CD69 on basophils might be useful as an in vitro as well as in vivo marker of activation of these cells by IL-3.
authors: Department of Allergy and Rheumatology, University of Tokyo Graduate School of Medicine, Tokyo, Japan.
authors: Chitose
authors: C
authors: Yoshimura
authors: Masao
authors: M
authors: Yamaguchi
authors: Motoyasu
authors: M
authors: Iikura
authors: Shinyu
authors: S
authors: Izumi
authors: Koichiro
authors: K
authors: Kudo
authors: Hiroyuki
authors: H
authors: Nagase
authors: Akira
authors: A
authors: Ishii
authors: Andrew F
authors: AF
authors: Walls
authors: Chisei
authors: C
authors: Ra
authors: Tsutomu
authors: T
authors: Iwata
authors: Takashi
authors: T
authors: Igarashi
authors: Kazuhiko
authors: K
authors: Yamamoto
authors: Koichi
authors: K
authors: Hirai
mesh_terms: D000368:Aged; D015703:Antigens, CD / Q000378:metabolism*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism*; D001249:Asthma / Q000097:blood; D001491:Basophils / Q000187:drug effects* / Q000276:immunology*; D015415:Biomarkers; D001773:Blood Cells / Q000378:metabolism; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D005260:Female; D006801:Humans; D018960:Hyaluronan Receptors / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D007377:Interleukin-3 / Q000494:pharmacology*; D037181:Lectins, C-Type; D008297:Male; D008875:Middle Aged; D013997:Time Factors; D015854:Up-Regulation; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D015415:Biomarkers; D018960:Hyaluronan Receptors; D018799:Intercellular Adhesion Molecule-1; D007377:Interleukin-3; D037181:Lectins, C-Type; D000099192:CD69 Antigens