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

Christine M. Deppong, Jian Xu, Steven L. Brody, Jonathan M. Green

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

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.

Original languageEnglish
Pages (from-to)L167-L173
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume302
Issue number1
DOIs
StatePublished - Jan 2012

Keywords

  • Lung inflammation
  • Lymphocyte proliferation
  • Lymphocytes

Fingerprint

Dive into the research topics of 'Airway epithelial cells suppress T cell proliferation by an IFNγ/STAT1/TGFβ-dependent mechanism'. Together they form a unique fingerprint.

Cite this