PMID- 15279568
OWN - NLM
STAT- MEDLINE
DCOM- 20041223
LR  - 20190823
IS  - 0929-8673 (Print)
IS  - 0929-8673 (Linking)
VI  - 11
IP  - 15
DP  - 2004 Aug
TI  - A molecular understanding of mast cell activation and the promise of 
      anti-allergic therapeutics.
PG  - 2083-91
AB  - Mast cells are central to allergic disease. Their immediate (exocytosis of 
      granule-stored allergic-mediators) and delayed (de novo synthesis of inflammatory 
      mediators) response to an allergen underlies the symptoms seen in acute; and 
      chronic allergic disease. Thus, intervention in the allergen-mediated activation 
      of mast cells is a long sought after goal in the treatment and management of 
      allergic disease. The recent gain in deciphering the molecular mechanisms 
      underlying immunoglobulin E (IgE)-mediated mast cell activation has provided 
      optimism for the development of new therapeutic strategies. Among the most 
      promising is the use of humanized anti-IgE antibodies that inhibit binding of IgE 
      to its high affinity receptor (FcepsilonRI) on the mast cell. Other strategies 
      target molecules proximal to FcepsilonRI, whose activities are central in mast 
      cell activation. One such molecule, Syk kinase, has been targeted by various 
      approaches including a small molecule inhibitor that specifically abrogates mast 
      cell degranulation. More recently, various molecules that function to promote 
      protein-protein interactions (adapters) were demonstrated as essential to mast 
      cell degranulation and cytokine production. It remains to be seen if these 
      molecules hold therapeutic promise for disease intervention. Additional studies 
      identifying molecules required for mast cell granule fusion and content 
      exocytosis also bodes well for discovery of new therapeutic targets. While our 
      understanding of IgE-mediated mast cell activation is still at its inception, the 
      modest success in identifying molecules essential to this process affords some 
      confidence for better treatment of allergic disease.
CI  - Copyright 2004 Bentham Science Publishers Ltd.
FAU - Kovarova, Martina
AU  - Kovarova M
AD  - Molecular Inflammation Section, Molecular Immunology and Inflammation Branch, 
      National Institute of Arthritis and Musculoskeletal and Skin Diseases, National 
      Institutes of Health, Bethesda, MD 20892, USA.
FAU - Rivera, Juan
AU  - Rivera J
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Med Chem
JT  - Current medicinal chemistry
JID - 9440157
RN  - 0 (Allergens)
RN  - 0 (Anti-Allergic Agents)
RN  - 0 (Receptors, IgE)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Allergens
MH  - Animals
MH  - Anti-Allergic Agents/*therapeutic use
MH  - Humans
MH  - Immunity, Cellular/drug effects
MH  - Immunoglobulin E/*immunology
MH  - Mast Cells/*immunology
MH  - Receptors, IgE/immunology
MH  - Respiratory Hypersensitivity/drug therapy/immunology
MH  - Signal Transduction
RF  - 108
EDAT- 2004/07/29 05:00
MHDA- 2004/12/24 09:00
CRDT- 2004/07/29 05:00
PHST- 2004/07/29 05:00 [pubmed]
PHST- 2004/12/24 09:00 [medline]
PHST- 2004/07/29 05:00 [entrez]
AID - 10.2174/0929867043364801 [doi]
PST - ppublish
SO  - Curr Med Chem. 2004 Aug;11(15):2083-91. doi: 10.2174/0929867043364801.