Activation of CFTR chloride current by nitric oxide in human T lymphocytes. |
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Authors: | Y J Dong A C Chao K Kouyama Y P Hsu R C Bocian R B Moss P Gardner |
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Affiliation: | Department of Molecular Pharmacology and Medicine, Stanford University School of Medicine, CA 94305, USA. |
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Abstract: | Nitric oxide, which is produced by cytokine-activated mononuclear cells, is thought to play an important role in inflammation and immunity. While the function of nitric oxide as a direct cytotoxic effector molecule is well established, its function as a transducer molecule in immune cells is not. By use of whole-cell patch clamp recordings, we show that nitric oxide activates cystic fibrosis transmembrane conductance regulator CI- currents in normal human cloned T cells by a cGMP-dependent mechanism. This pathway is defective in cystic fibrosis-derived human cloned T cells. These findings not only delineate a novel transduction mechanism for nitric oxide but also support the hypothesis that an intrinsic immune defect may exist in cystic fibrosis. |
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