TIM-1 mediates the induction of ozone-induced airway hyperreactivity through the recognition of apoptotic cells in the lung (120.33)
| Autor: | Hye Young Kim, HyunHee Lee, Ya-Jen Chang, Ya-Ting Chaung, Stephanie Shore, Gordon Freeman, Rosemarie DeKruyff, Dale Umetsu |
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| Rok vydání: | 2012 |
| Předmět: | |
| Zdroj: | The Journal of Immunology. 188:120.33-120.33 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.188.supp.120.33 |
| Popis: | Asthma is a heterogeneous inflammatory disease of the lungs that has multiple triggers, including air pollution. The mechanisms however, by which non-allergic triggers such as air pollution cause asthma are poorly understood. In a model of air pollution-induced asthma, we found that chronic exposure to ozone induced airway hyperreactivity (AHR), a cardinal feature of asthma, independently of adaptive immunity. The AHR induced by ozone was however, dependent on TIM-1, an important susceptibility gene for asthma and a receptor for phosphatidylserine (PtdSer), a marker of apoptotic cells. Moreover, ozone exposure caused apoptosis in airway epithelial cells, which triggerred AHR by activating TIM-1 expressing natural killer T (NKT) cells. These results demonstrate an important role for TIM-1 in asthma, in which AHR results from the activation of NKT cells sensing damaged/apoptotic airway epithelial cells through TIM-1. We thus define a novel innate pathway to experimental asthma that involves apoptosis and TIM-1, and that links airway injury to inflammation and AHR. |
| Databáze: | OpenAIRE |
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