Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9021286 | International Congress Series | 2005 | 5 Pages |
Abstract
Using NKT cell-deficient CD1d knockout and Jα281 knockout mice, we demonstrated that allergen-induced airway hyperreactivity (AHR), a cardinal feature of asthma, failed to develop in the absence of NKT cells. The failure of NKT cell-deficient mice to develop AHR was not due to an inability of these mice to develop Th2 responses and was reversed by adoptive transfer of tetramer purified NKT cells. These studies are the first to show that pulmonary NKT cells critically regulate the development of asthma and Th2-biased respiratory immunity against nominal exogenous antigens. In addition, our studies suggest that therapies that target NKT cells may be clinically effective in limiting the development of AHR and asthma.
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Authors
Dale T. Umetsu, Toshinori Nakayama, Masaru Taniguchi, Mitchell Kronenberg, Rosemarie H. DeKruyff, Omid Akbari,