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Airway epithelial cells prime plasmacytoid dendritic cells to respond to pathogens via secretion of growth factors

Mucosal Immunologyvolume 12pages7784 (2019) | Download Citation


  • A Correction to this article was published on 31 January 2019


Plasmacytoid dendritic cells (PDCs) are critical for defense against respiratory viruses because of their propensity to secrete high levels of type I interferons (IFN). The functions of PDCs in the lung can be influenced by airway epithelial cells. We examined the effect of human primary bronchial epithelial cells (PBECs) on PDC functions by performing RNA-sequencing of PDCs after co-culture with air liquid interface differentiated PBECs. Functional analysis revealed that PDCs co-cultured with PBECs displayed upregulation of type I IFN production and response genes. Upregulated transcripts included those encoding cytosolic sensors of DNA, ZBP-1,IRF-3, and NFkB as well as genes involved in amplification of the IFN response, such as IFNAR1, JAK/STAT, ISG15. In keeping with the RNA-seq data, we observe increased secretion of type I IFN and other cytokines in response to influenza in PDCs co-cultured with PBECs. The PDCs also primed Th1 responses in T cells. The enhanced response of PDCs co-cultured with PBECs was due to the action of growth factors, GMCSF, GCSF, and VEGF, which were secreted by PBECs on differentiation. These data highlight possible mechanisms to enhance the production of type-I IFN in the airways, which is critical for host defense against respiratory infections.

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  • 31 January 2019

    The original version of this Article contained an error in the spelling of the author Hannah Nguyen, which was incorrectly given as Hannah Ngyuen. This has now been corrected in both the PDF and HTML versions of the Article.


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This study was supported by grant from the NIH AG045216 (to AA), and from the National Center for Research Resources and the National Center for Advancing Translational Sciences # UL1 TR000153. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. We are grateful to ICTS UC Irvine for providing the blood samples.

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Author notes

  1. These authors contributed equally: Farah Rahmatpanah, Sudhanshu Agrawal, Natasha Jaiswal


  1. Department of pathology, University of California, Irvine, CA, 92697, USA

    • Farah Rahmatpanah
  2. Division of Basic and Clinical Immunology, Department of Medicine, University of California, Irvine, CA, 92697, USA

    • Sudhanshu Agrawal
    • , Natasha Jaiswal
    • , Hannah M. Nguyen
    •  & Anshu Agrawal
  3. Microbiology & Molecular Genetics, University of California, Irvine, CA, 92697, USA

    • Michael McClelland


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F.R. performed sequencing analysis, N.J. performed the functional studies, S.A. sorted pDCs for sequencing and helped perform functional studies, H.N. helped in cell purification, M.M. helped in sequencing analysis, A.A. wrote the manuscript and supervised the experiments. All authors helped in the discussing and editing of manuscript.

Competing interests

The authors declare no competing interests.

Corresponding author

Correspondence to Anshu Agrawal.

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