title: Effect of omalizumab treatment on peripheral eosinophil and T-lymphocyte function in patients with allergic asthma.
abstract: BACKGROUND
  Omalizumab is a recombinant monoclonal anti-IgE antibody with proven efficacy in allergic diseases and further anti-inflammatory potency in the treatment of asthma.
  
  
  OBJECTIVE
  To explore the anti-inflammatory mechanism of omalizumab, we investigated the induction of immunologic changes leading to eosinophil apoptosis and examined T-lymphocyte cytokine profiles in patients with allergic asthma.
  
  
  METHODS
  Nineteen patients with allergic asthma were enrolled and received omalizumab at a dose of at least 0.016 mg/kg/IgE (IU/mL) every 4 weeks. Peripheral eosinophils and T-lymphocyte cytokine profiles were evaluated by fluorescence-activated cell sorting before treatment (baseline), at 12 weeks of treatment, and 12 weeks after discontinuation of treatment with omalizumab or placebo.
  
  
  RESULTS
  Markers of eosinophil apoptosis (Annexin V) were significantly increased in omalizumab recipients compared with placebo, whereas no changes in markers of necrosis (7-amino-actinomycin) or eosinophil activation CD69 or Fas receptor (CD95) were detected. GM-CSF+ lymphocytes were reduced in omalizumab recipients compared with placebo. Fewer IL-2+ and IL-13+ lymphocytes were evident in omalizumab recipients than in the placebo group. There were no significant differences in IL-5, IFN-gamma, or TNF-alpha between the omalizumab and placebo groups.
  
  
  CONCLUSIONS
  These findings provide further evidence that omalizumab has additional anti-inflammatory activity demonstrated by induction of eosinophil apoptosis and downregulation of the inflammatory cytokines IL-2 and IL-13. Further studies are needed to determine the underlying mechanisms.
  
  
  CONCLUSIONS
  These findings support the critical role of IgE in the regulation of inflammation in allergic asthma: influencing the inflammation is the key to control the more severe type of asthma.
authors.affiliation: Department of Internal Medicine, Charité Universitätsmedizin Berlin, Germany. oliver.noga@charite.de
authors.forename: Oliver
authors.initials: O
authors.lastname: Noga
authors.forename: Gerald
authors.initials: G
authors.lastname: Hanf
authors.forename: Ilka
authors.initials: I
authors.lastname: Brachmann
authors.forename: Andrea C
authors.initials: AC
authors.lastname: Klucken
authors.forename: Jörg
authors.initials: J
authors.lastname: Kleine-Tebbe
authors.forename: Simone
authors.initials: S
authors.lastname: Rosseau
authors.forename: Gert
authors.initials: G
authors.lastname: Kunkel
authors.forename: Norbert
authors.initials: N
authors.lastname: Suttorp
authors.forename: Joachim
authors.initials: J
authors.lastname: Seybold
mesh_terms: D000328:Adult; D000368:Aged; D000485:Allergens / Q000276:immunology*; D018927:Anti-Asthmatic Agents / Q000494:pharmacology*; D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D061067:Antibodies, Monoclonal, Humanized; D017209:Apoptosis / Q000187:drug effects / Q000276:immunology; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology* / Q000473:pathology; D016207:Cytokines / Q000378:metabolism; D004804:Eosinophils / Q000187:drug effects* / Q000276:immunology / Q000473:pathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D000069444:Omalizumab; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology* / Q000378:metabolism
chemical_list: D000485:Allergens; D018927:Anti-Asthmatic Agents; D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D016207:Cytokines; D000069444:Omalizumab