Journal
JOURNAL OF IMMUNOLOGY
Volume 183, Issue 12, Pages 8203-8215Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0900646
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Funding
- MEXT (Monbukagakusho) (Japan)
- Ministry of Education, Culture, Sports. Science and Technology (Japan) [17016010, 20060003, 17390139, 18590466, 19590491, 19591609, 20590485, 19659121, 20790367, 20890038]
- Special Coordination Funds for Promoting Science and Technology
- Cancer Translational Research Project
- Ministry of Health, Labor and Welfare (Japan)
- Japan Health Science Foundation
- Naito Foundation
- Grants-in-Aid for Scientific Research [19590491, 20590485, 20060003, 20790367, 19659121, 17390139, 21591808, 21390147, 20890038, 18590466, 19591609] Funding Source: KAKEN
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Airway inflammation and airway hyperresponsiveness are central issues in the pathogenesis of asthma. CD69 is a membrane molecule transiently expressed on activated lymphocytes, and its selective expression in inflammatory infiltrates suggests that it plays a role in the pathogenesis of inflammatory diseases. In CD69-deficient mice, OVA-induced eosinophilic airway inflammation, mucus hyperproduction, and airway hyperresponsiveness were attenuated. Cell transfer of Ag-primed wild-type but not CD69-deficient CD4 T cells restored the induction of allergic inflammation in CD69-deficient mice, indicating a critical role of CD69 expressed on CD4 T cells. Th2 responses induced by CD69-deficient CD4 T cells in the lung were attenuated, and the migration of CD4 T cells into the asthmatic lung was severely compromised. The expression of VCAM-1 was also substantially altered, suggesting the involvement of VCAM-I in the CD69-dependent migration of Th2 cells into the asthmatic lung. Interestingly, the administration of anti-CD69 Ab inhibited the induction of the OVA-induced airway inflammation and hyperresponsiveness. This inhibitory effect induced by the CD69 mAb was observed even after the airway challenge with OVA. These results indicate that CD69 plays a crucial role in the pathogenesis of allergen-induced eosinophilic airway inflammation and hyperresponsiveness and that CD69 could be a possible therapeutic target for asthmatic patients. The Journal of Immunology, 2009, 183: 8203-8215.
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