title: Evidence of in vivo basophil activation in chronic idiopathic urticaria.
abstract: BACKGROUND
  Approximately 40% of chronic idiopathic urticaria (CIU) subjects have autoantibodies to either FcepsilonRIalpha or IgE. The effect of such autoantibodies on circulating basophil activation status is unknown.
  
  
  OBJECTIVE
  The expression of cell surface activation markers on basophils from CIU, non-allergic, and allergic subjects were compared. Further, the relationship between marker expression and serum factors reported in CIU, such as histamine-releasing activity (HRA) and immunoreactivity to FcepsilonRIalpha were examined.
  
  
  METHODS
  Peripheral blood was obtained from CIU, allergic, and non-allergic donors and fractionated by density gradients. Enriched basophils (1-12%) were analysed by flow cytometry for expression of activation markers including CD63, CD69, and CD203c. Dilutions of serum (5-50%) were analysed for HRA on basophils from a normal donor. Serum was tested for immunoreactivity by western blotting to a standard cell lysate prepared from an RBL-SX38 cell line transfected with human FcepsilonRIalpha.
  
  
  RESULTS
  CIU subjects (n=9) and allergic subjects (n=8) exhibited enhanced expression of CD63 and CD69, as compared with non-allergic subjects (n=7); however, no difference was seen among groups for CD203c expression. Five CIU and two non-allergic subjects had evidence of significant serum HRA (>20%), whereas two CIU, two allergic, and three non-allergic subjects had evidence of serum immunoreactivity to FcepsilonRIalpha. Serum HRA and serum immunoreactivity to FcepsilonRIalpha were not associated with enhanced surface marker expression.
  
  
  CONCLUSIONS
  Basophil activation marker expression is increased in CIU subjects and is not associated with serum factors. In addition, serum HRA and FcepsilonRIalpha immunoreactivity are not unique to CIU, or related to enhanced circulating basophil marker expression.
authors.affiliation: Department of Medicine, Division of Allergy and Clinical Immunology, The Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.
authors.forename: K
authors.initials: K
authors.lastname: Vasagar
authors.forename: B M
authors.initials: BM
authors.lastname: Vonakis
authors.forename: L M
authors.initials: LM
authors.lastname: Gober
authors.forename: A
authors.initials: A
authors.lastname: Viksman
authors.forename: S P
authors.initials: SP
authors.lastname: Gibbons
authors.forename: S S
authors.initials: SS
authors.lastname: Saini
mesh_terms: D015703:Antigens, CD / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D001491:Basophils / Q000276:immunology*; D015415:Biomarkers / Q000032:analysis; D016022:Case-Control Studies; D002908:Chronic Disease; D005434:Flow Cytometry; D006636:Histamine Release; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology; D007377:Interleukin-3 / Q000494:pharmacology; D037181:Lectins, C-Type; D010980:Platelet Membrane Glycoproteins / Q000032:analysis; D017455:Receptors, IgE / Q000097:blood; D060149:Tetraspanin 30; D014581:Urticaria / Q000097:blood / Q000276:immunology*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D015415:Biomarkers; D007377:Interleukin-3; D037181:Lectins, C-Type; D010980:Platelet Membrane Glycoproteins; D017455:Receptors, IgE; D060149:Tetraspanin 30; D000099192:CD69 Antigens; C554586:CD63 protein, human; C475664:FCER1A protein, human