Abstract
Organ-specific regulation of immune responses relies on the exchange of information between nonimmune and immune cells. In a primary culture model of the lung airway, we demonstrate that T cell proliferation is potently inhibited by airway epithelial cells (ECs). This is mediated by activation of the IFNγ/STAT1 pathway in the EC and transforming growth factor-β (TGFβ)-dependent suppression of T cell proliferation. In this way, the EC can restrict the expansion of T cells. Given the constant exposure of the airway to inhaled antigen, this may be important in setting a threshold for the initiation of T cell-dependent immune responses and preventing unwanted, chronic inflammation.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cell Proliferation
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Coculture Techniques
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Epithelial Cells* / immunology
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Epithelial Cells* / metabolism
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Interferon-gamma* / immunology
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Interferon-gamma* / metabolism
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Lymphocyte Activation / immunology
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Mice
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Mice, Inbred C57BL
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Pneumonia / immunology
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Pneumonia / physiopathology
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STAT1 Transcription Factor* / immunology
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STAT1 Transcription Factor* / metabolism
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Signal Transduction / immunology
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T-Lymphocytes* / immunology
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T-Lymphocytes* / metabolism
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Trachea / cytology
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Trachea / immunology
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Trachea / metabolism
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Transforming Growth Factor beta* / immunology
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Transforming Growth Factor beta* / metabolism
Substances
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STAT1 Transcription Factor
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Stat1 protein, mouse
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Transforming Growth Factor beta
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Interferon-gamma