Airway epithelial cells suppress T cell proliferation by an IFNγ/STAT1/TGFβ-dependent mechanism.

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.

• Authors: Christine M Deppong, Jian Xu, Steven L Brody, Jonathan M Green
• Journal: American journal of physiology. Lung cellular and molecular physiology (Am J Physiol Lung Cell Mol Physiol) Vol. 302 Issue 1 Pg. L167-73 (Jan 01 2012) ISSN: 1522-1504 [Electronic] United States
• PMID: 22003092 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• STAT1 Transcription Factor
• Stat1 protein, mouse
• Transforming Growth Factor beta
• Interferon-gamma

Topics

• Animals
• Cell Proliferation
• Coculture Techniques
• Epithelial Cells (immunology, metabolism)
• Interferon-gamma (immunology, metabolism)
• Lymphocyte Activation (immunology)
• Mice
• Mice, Inbred C57BL
• Pneumonia (immunology, physiopathology)
• STAT1 Transcription Factor (immunology, metabolism)
• Signal Transduction (immunology)
• T-Lymphocytes (immunology, metabolism)
• Trachea (cytology, immunology, metabolism)
• Transforming Growth Factor beta (immunology, metabolism)