التفاصيل البيبلوغرافية
| العنوان: |
T-cell immunoglobulin and mucin domain 1 deficiency eliminates airway hyperreactivity triggered by the recognition of airway cell death. |
| المؤلفون: |
Kim, Hye Young, Chang, Ya-Jen, Chuang, Ya-Ting, Lee, Hyun-Hee, Kasahara, David I., Martin, Thomas, Hsu, Joyce T., Savage, Paul B., Shore, Stephanie A., Freeman, Gordon J., DeKruyff, Rosemarie H., Umetsu, Dale T. |
| المصدر: |
Journal of Allergy & Clinical Immunology; Aug2013, Vol. 132 Issue 2, p414-425.e6, 0p |
| مستخلص: |
Background: Studies of asthma have been limited by a poor understanding of how nonallergic environmental exposures, such as air pollution and infection, are translated in the lung into inflammation and wheezing. Objective: Our goal was to understand the mechanism of nonallergic asthma that leads to airway hyperreactivity (AHR), a cardinal feature of asthma independent of adaptive immunity. Method: We examined mouse models of experimental asthma in which AHR was induced by respiratory syncytial virus infection or ozone exposure using mice deficient in T-cell immunoglobulin and mucin domain 1 (TIM1/HAVCR1), an important asthma susceptibility gene. Results: TIM1 −/− mice did not have airways disease when infected with RSV or when repeatedly exposed to ozone, a major component of air pollution. On the other hand, the TIM1 −/− mice had allergen-induced experimental asthma, as previously shown. The RSV- and ozone-induced pathways were blocked by treatment with caspase inhibitors, indicating an absolute requirement for programmed cell death and apoptosis. TIM-1–expressing, but not TIM-1–deficient, natural killer T cells responded to apoptotic airway epithelial cells by secreting cytokines, which mediated the development of AHR. Conclusion: We defined a novel pathway in which TIM-1, a receptor for phosphatidylserine expressed by apoptotic cells, drives the development of asthma by sensing and responding to injured and apoptotic airway epithelial cells. [Copyright &y& Elsevier] |
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| قاعدة البيانات: |
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