title: Induction of apoptosis in human basophils by anti-Fas antibody treatment in vitro.
abstract: BACKGROUND
  Basophils are thought to play an important role in the pathogenesis of allergic inflammation; however, the factors associated with basophil death are not fully understood. Fas (CD95) is a member of the TNF receptor superfamily and is known to induce apoptosis in activated T cells, neutrophils and eosinophils. In the present study, the expression and function of Fas in human basophils were investigated in vitro.
  
  
  METHODS
  Human cultured basophils were obtained by culturing cord blood-derived CD34+ cells in the presence of 2.5 ng/ml of IL-3 for 5-6 weeks. The expression of Fas was measured using flow cytometry. Cell viability and morphological changes after the incubation of basophils with anti-Fas mAb (clone CH11, IgM) in the presence of 1 ng/ml of IL-3 were measured using the trypan blue dye exclusion test and light microscopy, respectively.
  
  
  RESULTS
  Human cultured basophils constitutively and significantly expressed Fas on their cell surfaces. Treatment with anti-Fas monoclonal antibody (mAb) significantly reduced basophil viability in a time- and dose-dependent manner. When basophils were incubated with 10 ng/ml of anti-Fas mAb or control for 72 h, the basophil viability was 27.3 +/- 8.8% and 89.3 +/- 5.2%, respectively (p < 0.01). Anti-Fas mAb-treated basophils were shrunken and exhibited condensed nuclei, consistent with apoptosis.
  
  
  CONCLUSIONS
  Our findings indicate that human basophils express functional Fas on their cell surfaces, and signaling via Fas may regulate basophil survival in vivo.
authors.affiliation: Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan. kmatsumoto@nch.go.jp
authors.forename: Kenji
authors.initials: K
authors.lastname: Matsumoto
authors.forename: Akihiko
authors.initials: A
authors.lastname: Maeda
authors.forename: Bruce S
authors.initials: BS
authors.lastname: Bochner
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Wakiguchi
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Saito
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D058846:Antibodies, Monoclonal, Murine-Derived; D017209:Apoptosis / Q000276:immunology*; D001491:Basophils / Q000187:drug effects / Q000276:immunology*; D002470:Cell Survival; D002478:Cells, Cultured; D004306:Dose-Response Relationship, Immunologic; D005434:Flow Cytometry; D006801:Humans; D019014:fas Receptor / Q000096:biosynthesis / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; D058846:Antibodies, Monoclonal, Murine-Derived; C411023:anti-Fas monoclonal antibody; D019014:fas Receptor