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Airway epithelial cells suppress T cell proliferation by an IFNγ/STAT1/TGFβ-dependent mechanism
Author(s) -
Christine Deppong,
Jian Xu,
Steven L. Brody,
Jonathan M. Green
Publication year - 2011
Publication title -
ajp lung cellular and molecular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.892
H-Index - 163
eISSN - 1522-1504
pISSN - 1040-0605
DOI - 10.1152/ajplung.00188.2011
Subject(s) - stat1 , immune system , transforming growth factor , microbiology and biotechnology , cell growth , immunology , airway , inflammation , biology , t cell , cell , lung , cancer research , signal transduction , medicine , genetics , surgery
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.

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