期刊
JOURNAL OF IMMUNOLOGY
卷 181, 期 9, 页码 6557-6562出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.9.6557
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类别
资金
- National Institutes of Health [AI44259, AI68731, AI71130]
- Department of Defense [USAMRAA W81XWH-07-0246]
- American Lung Association
- National Cancer Institute [T32, CA009537]
Lung-specific thymic stromal lymphopoietin (TSLP) expression is sufficient for the development of an asthma-like chronic airway inflammatory disease. However, the nature of the downstream pathways that regulate disease development are not known. In this study, we used IL-4- and Stat6-deficient mice to establish the role of Th2-type responses downstream of TSLP. IL-4 deficiency greatly reduced, but did not eliminate, TSLP-induced airway hyperresponsiveness, airway inflammation, eosinophilia, and goblet cell metaplasia, while Stat6 deficiency eliminated these asthma-like symptoms. We further demonstrate, using the chronic model of TSLP-mediated airway inflammation, that blockade of both IL-4 and IL-13 responses, through administration of an anti-IL-4R alpha mAb, reversed asthma-like symptoms, when given to mice with established disease. Collectively these data provide insight into the pathways engaged in TSLP-driven airway inflammation and demonstrate that simultaneous blockade of IL-4 and IL-13 can reverse established airway disease, suggesting that this may be an effective approach for the therapy of Th2-mediated inflammatory respiratory disease. The Journal of Immunology, 2008, 181: 6557-6562.
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