PMID- 15379589
OWN - NLM
STAT- MEDLINE
DCOM- 20041228
LR  - 20220330
IS  - 1568-010X (Print)
IS  - 1568-010X (Linking)
VI  - 3
IP  - 3
DP  - 2004 Sep
TI  - Anti-IgE monoclonal antibody (omalizumab) in the treatment of atopic asthma and 
      allergic respiratory diseases.
PG  - 227-9
AB  - Since the discovery of immunoglobulin E (IgE) antibodies thirty-six years ago, 
      our understanding of the mechanisms of allergy has improved to such an extent 
      that we can now better differentiate allergy from non-allergic hypersensitivity, 
      and allergic/atopic from intrinsic/non-atopic bronchial asthma. IgE antibodies 
      are crucial immune mediators of airway inflammation in allergic atopic asthma and 
      IgE-mediated hypersensitivity reactions are the likely mechanisms of 
      allergen-induced airway obstruction. In addition, IgE may cause chronic airway 
      inflammation in asthma through effector cells activated via high-affinity 
      (Fcepsilon RI) or low-affinity (Fcepsilon RII) IgE receptors. Therapeutic 
      anti-IgE antibodies able to reduce free IgE levels and to block the binding of 
      IgE to Fcepsilon RI without cross-linking IgE and triggering degranulation of 
      IgE-sensitised cells have been developed. This non-anaphylactogenic anti-IgE 
      monoclonal antibody (rhuMAb-E25; omalizumab) binds IgE at the same site as these 
      antibodies bind Fcepsilon RI and Fcepsilon RII. As a consequence, omalizumab 
      inhibits IgE effector functions by blocking IgE binding to high-affinity 
      receptors on IgE effector cells and does not cause mast cell or basophil 
      activation because it cannot bind to IgE on cell surfaces where the Fcepsilon R1 
      receptor already masks the anti-IgE epitope. Studies in patients with atopic 
      asthma demonstrated that omalizumab decreases serum IgE levels and 
      allergen-induced bronchoconstriction during both the early and late-phase 
      responses to inhaled allergen. In several clinical controlled trials omalizumab 
      resulted to be able to reduce asthma-related symptoms, to decrease corticosteroid 
      use and to improve quality of life of asthmatic patients. The anti-IgE approach 
      to asthma treatment has several advantages, including concomitant treatment of 
      other IgE-mediated diseases (allergic rhinitis, allergic conjunctivitis, atopic 
      dermatitis and food allergies), a favourable side-effect profile and a 
      twice-monthly dosing frequency.
FAU - D'Amato, Gennaro
AU  - D'Amato G
AD  - Division of Respiratory and Allergic Diseases, Department of Chest Diseases, High 
      Speciality Hospital A Cardarelli, Naples, Italy. gdamato@qubisoft.it
FAU - Liccardi, Gennaro
AU  - Liccardi G
FAU - Noschese, Paolo
AU  - Noschese P
FAU - Salzillo, Antonello
AU  - Salzillo A
FAU - D'Amato, Maria
AU  - D'Amato M
FAU - Cazzola, Mario
AU  - Cazzola M
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Netherlands
TA  - Curr Drug Targets Inflamm Allergy
JT  - Current drug targets. Inflammation and allergy
JID - 101160019
RN  - 0 (Anti-Allergic Agents)
RN  - 0 (Antibodies, Anti-Idiotypic)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 2P471X1Z11 (Omalizumab)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Anti-Allergic Agents/pharmacology/*therapeutic use
MH  - Antibodies, Anti-Idiotypic
MH  - Antibodies, Monoclonal/pharmacology/*therapeutic use
MH  - Antibodies, Monoclonal, Humanized
MH  - Asthma/drug therapy/immunology
MH  - Clinical Trials as Topic
MH  - Humans
MH  - Hypersensitivity/*drug therapy/immunology
MH  - Immunoglobulin E/*immunology
MH  - Omalizumab
RF  - 20
EDAT- 2004/09/24 05:00
MHDA- 2004/12/29 09:00
CRDT- 2004/09/24 05:00
PHST- 2004/09/24 05:00 [pubmed]
PHST- 2004/12/29 09:00 [medline]
PHST- 2004/09/24 05:00 [entrez]
AID - 10.2174/1568010043343615 [doi]
PST - ppublish
SO  - Curr Drug Targets Inflamm Allergy. 2004 Sep;3(3):227-9. doi: 
      10.2174/1568010043343615.