title: Omalizumab decreased IgE-release and induced changes in cellular immunity in patients with allergic asthma.
abstract: BACKGROUND
  Omalizumab, a recombinant monoclonal anti-immunoglobulin E (IgE) antibody, shows proven efficacy in the treatment of allergic diseases. A little is known about the immunological pathways affected by the decrease of circulating free IgE during omalizumab treatment.
  
  
  OBJECTIVE
  To investigate the immunological consequence of IgE withdrawal, we studied the influence of omalizumab on stimulated IgE-release of cultured peripheral blood mononuclear cells (PBMC) and on the relative number of lymphocytes in the peripheral blood (cellular immune status) in patients with allergic asthma.
  
  
  METHODS
  Nineteen patients were enrolled and received omalizumab at a dose of at least 0.016 mg/kg/IgE (IU/ml) every 4 weeks. PBMC were isolated from peripheral blood. Cells were cultured and stimulated with IL-4 (5 ng/ml) and CD40 ligand (1 microg/ml) for 10 days. IgE release was detected in cell culture supernatants by enzyme-linked immunosorbent assay (ELISA). Cellular immune status was investigated by fluorescence-activated cell sorting.
  
  
  RESULTS
  Omalizumab treatment induced significant inhibition of stimulated IgE release (median 1.38-0 ng/ml vs. 1.64-2.0 ng/ml in placebo group, P<0.05). B-lymphocyte counts were also significantly lower in the omalizumab group compared with placebo after 12 weeks of treatment (median 18.2-15.6% lymphocytes vs 12.7-13.7% lymphocytes after placebo, P<0.01). There were no significant differences in the other lymphocyte subpopulations between the groups.
  
  
  CONCLUSIONS
  These findings provide evidence of immunological influences of omalizumab treatment, leading to a downregulation of IgE secretion and decrease of lymphocyte subpopulations (B-cells) indicating their anti-inflammatory potency.
authors.affiliation: Department of Internal Medicine, Charité- Universitätsmedizin Berlin, Berlin, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Hanf
authors.forename: I
authors.initials: I
authors.lastname: Brachmann
authors.forename: J
authors.initials: J
authors.lastname: Kleine-Tebbe
authors.forename: J
authors.initials: J
authors.lastname: Seybold
authors.forename: G
authors.initials: G
authors.lastname: Kunkel
authors.forename: N
authors.initials: N
authors.lastname: Suttorp
authors.forename: O
authors.initials: O
authors.lastname: Noga
mesh_terms: D000328:Adult; D000368:Aged; D000485:Allergens / Q000009:adverse effects* / Q000276:immunology*; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D061067:Antibodies, Monoclonal, Humanized; D001249:Asthma / Q000276:immunology* / Q000378:metabolism / Q000628:therapy*; D005260:Female; D006801:Humans; D007111:Immunity, Cellular; D007073:Immunoglobulin E / Q000378:metabolism*; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D000069444:Omalizumab
chemical_list: D000485:Allergens; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000888:Antibodies, Anti-Idiotypic; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000069444:Omalizumab; D007073:Immunoglobulin E