Activation of CFTR chloride current by nitric oxide in human T lymphocytes.

AUTOR(ES)

Dong, Y J

RESUMO

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.

Documentos Relacionados

• Novel activation stimulus of chloride channels by potassium in human osteoblasts and human leukaemic T lymphocytes.
• Activation of c-myb expression by phytohemagglutinin stimulation in normal human T lymphocytes.
• Regulation of Human Immunodeficiency Virus Type 1 Replication in Human T Lymphocytes by Nitric Oxide
• Activation of human blood monocytes by products of sensitized lymphocytes.
• Transcriptional activation of the human cytotoxic serine protease gene CSP-B in T lymphocytes.