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Asthma, allergy and chemokines
1Leukocyte Biology Section, Biomedical Sciences Division, Sir Alexander Fleming Building, Imperial College London, Exhibition Road, London SW7 2AZ, UK. j.pease@imperial.ac.uk
Current Drug Targets
|February 4, 2006
Summary
Targeting the CCR3:eotaxin axis can treat asthma by blocking eosinophil recruitment. This review explores chemokines and their receptors in allergic inflammation.
Area of Science:
- Immunology
- Allergy Research
- Molecular Biology
Background:
- Chemokines are cytokines that guide leukocyte subsets via G protein-coupled receptors.
- Allergen exposure upregulates specific chemokines, driving leukocyte recruitment in allergic inflammation.
- The chemokine receptor CCR3 is key in recruiting eosinophils, Th2 lymphocytes, basophils, and mast cells.
Purpose of the Study:
- To review recent advancements in chemokine and chemokine receptor research related to allergic inflammation.
- To highlight the role of the CCR3:eotaxin axis in eosinophil recruitment.
- To discuss other chemokine:chemokine receptor axes involved in allergic responses.
Main Methods:
- Literature review of recent developments in chemokine research.
- Analysis of the CCR3:eotaxin axis and its role in eosinophil recruitment.
- Examination of other implicated chemokine:chemokine receptor pathways.
Main Results:
- CCR3 binds eotaxins (CCL11, CCL24, CCL26), which are upregulated post-allergen challenge.
- Eosinophils, recruited via CCR3, contribute to tissue repair, remodeling, and damage.
- Blockade of the CCR3:eotaxin axis is a potential therapeutic strategy for asthma.
Conclusions:
- The CCR3:eotaxin pathway is critical for eosinophil-mediated allergic inflammation.
- Targeting this axis offers a promising therapeutic avenue for asthma treatment.
- Further research into other chemokine axes is essential for a comprehensive understanding of allergic inflammation.