Send to

Choose Destination
See comment in PubMed Commons below
Crit Rev Clin Lab Sci. 2004;41(1):79-113.

Biochemical assessment of intracellular signal transduction pathways in eosinophils: implications for pharmacotherapy.

Author information

  • 1Department of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, NT, Hong Kong.


Allergic asthma and allergic rhinitis are inflammatory diseases of the airway. Cytokines and chemokines produced by T helper (Th) type 2 cells (GM-CSF, IL-4, IL-5, IL-6, IL-9, IL-10 and IL-13), eotaxin, transforming growth factor-beta, and IL-11 orchestrate most pathophysiological processes of the late-phase allergic reaction, including the recruitment, activation, and delayed apoptosis of eosinophils, as well as eosinophilic degranulation to release eosinophilic cationic protein, major basic protein, and eosinophil-derived neurotoxin. These processes are regulated through an extensive network of interactive intracellular signal transduction pathways that have been intensively investigated recently. Our present review updates the cytokine and chemokine-mediated signal transduction mechanisms including the RAS-RAF-mitogen-activated protein kinases, Janus kinases (signal transducers and activators of transcription), phosphatidylinositol 3-kinase, nuclear factor-kappa B, activator protein-1, GATA, and cyclic AMP-dependent pathways, and describes the roles of different signaling pathways in the regulation of eosinophil differentiation, recruitment, degranulation, and expression of adhesion molecules. We shall also discuss different biochemical methods for the assessment of various intracellular signal transduction molecules, and various antagonists of receptors, modulators, and inhibitors of intracellular signaling molecules, many of which are potential therapeutic agents for treating allergic diseases.

[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Taylor & Francis
    Loading ...
    Support Center