Literature DB >> 22003092

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

Christine M Deppong1, Jian Xu, Steven L Brody, Jonathan M Green.   

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.

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Year:  2011        PMID: 22003092      PMCID: PMC3349368          DOI: 10.1152/ajplung.00188.2011

Source DB:  PubMed          Journal:  Am J Physiol Lung Cell Mol Physiol        ISSN: 1040-0605            Impact factor:   5.464


  28 in total

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9.  Loss of integrin alpha(v)beta6-mediated TGF-beta activation causes Mmp12-dependent emphysema.

Authors:  David G Morris; Xiaozhu Huang; Naftali Kaminski; Yanli Wang; Steven D Shapiro; Gregory Dolganov; Adam Glick; Dean Sheppard
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10.  The integrin alpha(v)beta8 mediates epithelial homeostasis through MT1-MMP-dependent activation of TGF-beta1.

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Journal:  J Immunol       Date:  2016-02-29       Impact factor: 5.422

2.  A detailed phenotypic analysis of immune cell populations in the bronchoalveolar lavage fluid of atopic asthmatics after segmental allergen challenge.

Authors:  Jonathan S Boomer; Amit D Parulekar; Brenda M Patterson; Huiqing Yin-Declue; Christine M Deppong; Seth Crockford; Nizar N Jarjour; Mario Castro; Jonathan M Green
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