Document Detail

Intracellular signal transduction in eosinophils and its clinical significance.
MedLine Citation:
PMID:  12066845     Owner:  NLM     Status:  MEDLINE    
The incidence and prevalence of allergic diseases such as asthma and allergic rhinitis have recently been increasing worldwide. Eosinophils are the principal effector cells for the pathogenesis of allergic inflammation via the secretion of highly cytotoxic granular proteins including eosinophil cationic protein, major basic protein and eosinophil protein X. Blood and tissue eosinophilia is a common manifestation of late-phase allergic inflammation causing tissue damage. The development of eosinophilia correlates with the production of haematopoietic cytokines including interleukin (IL)-3. IL-5 and granulocyte macrophage colony stimulating factor (GM-CSF), and eosinophil-specific chemoattractant, eotaxin, from T-lymphocytes and the epithelium respectively. Elucidation of intracellular mechanisms that control the activation, apoptosis and recruitment of eosinophils to tissues is therefore fundamental in understanding these disease processes and provides targets for novel drug therapy. Over the past decade, there has been intensive investigation for the intracellular signal transduction regulating various biological functions of eosinophils and their roles in the pathogenesis of eosinophil-related diseases. This review will emphasize on the cytokine and chemokine-mediated signal transductions including the RAS-RAF-mitogen-activated protein kinases (MAPK), Janus kinases (JAK)-signal transducers and activators of transcription (STAT), phosphatidylinositol 3-kinase (PI3K) and nuclear factor-kappa B (NF-kappaB), and various antagonists of receptors and inhibitors of intracellular signaling molecules as potential therapeutic agents of allergic diseases.
Chun Kwok Wong; Jiping Zhang; Wai Ki Ip; Christopher Wai Kei Lam
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Immunopharmacology and immunotoxicology     Volume:  24     ISSN:  0892-3973     ISO Abbreviation:  Immunopharmacol Immunotoxicol     Publication Date:  2002 May 
Date Detail:
Created Date:  2002-06-17     Completed Date:  2003-01-07     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8800150     Medline TA:  Immunopharmacol Immunotoxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  165-86     Citation Subset:  IM    
Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT.
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MeSH Terms
1-Phosphatidylinositol 3-Kinase / metabolism
Chemotactic Factors, Eosinophil / metabolism
Eosinophils / immunology*,  physiology*
Hypersensitivity / therapy
Intracellular Fluid / immunology
Mitogen-Activated Protein Kinases / metabolism
Models, Immunological
NF-kappa B / metabolism
Receptors, Cytokine / metabolism
Signal Transduction
Reg. No./Substance:
0/Chemotactic Factors, Eosinophil; 0/NF-kappa B; 0/Receptors, Cytokine; EC 3-Kinase; EC Protein Kinases

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