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CCR4 blockade does not inhibit allergic airways inflammation.
Dolores M Conroy1, Louise A Jopling, Clare M Lloyd
1Leukocyte Biology Section, Biomedical Sciences Division, Faculty of Medicine, Imperial College, London, United Kingdom.
Journal of Leukocyte Biology
|September 10, 2003
Summary
CC chemokine receptor 4 (CCR4) blockade did not significantly impact T-cell recruitment or inflammation in allergic asthma models. These findings question CCR4
Area of Science:
- Immunology
- Respiratory Medicine
- Allergy Research
Background:
- CC chemokine receptor 4 (CCR4) is implicated in T-cell recruitment, particularly T helper type 2 (Th2) cells.
- CCR4+ T cells are observed in the asthmatic lung, but their precise role in allergic airways inflammation is unclear.
Purpose of the Study:
- To investigate the role of CCR4 in allergic airways inflammation using a guinea pig model.
- To determine if CCR4 blockade affects Th2 cell recruitment and inflammatory responses in the lung.
Main Methods:
- Administered a CCR4-specific antibody to allergen-challenged guinea pigs.
- Analyzed bronchoalveolar lavage fluid for CCR4+ T cells.
- Measured levels of eotaxin/CCL11 and macrophage-derived chemokine/CCL22.
- Assessed the recruitment of inflammatory leukocytes to the lung.
Main Results:
- CCR4 blockade resulted in minimal changes in CCR4+ T cells in bronchoalveolar lavage fluid.
- Blockade failed to inhibit the generation of eotaxin/CCL11 or macrophage-derived chemokine/CCL22.
- Inflammatory leukocyte recruitment to the lung was not significantly inhibited by CCR4 blockade.
Conclusions:
- Antigen-specific Th2 cells are recruited to the lung via pathways other than CCR4.
- CCR4 may not be a reliable marker for Th2 cell recruitment in asthma.
- The study casts doubt on the therapeutic potential of targeting CCR4 for asthma treatment.