Control of pathogenic effector T-cell activities in situ by PD-L1 expression on respiratory inflammatory dendritic cells during respiratory syncytial virus infection

S. Yao, L. Jiang, E. K. Moser, L. B. Jewett, J. Wright, J. Du, B. Zhou, S. D. Davis, N. L. Krupp, T. J. Braciale, J. Sun

Research output: Contribution to journalArticle

26 Scopus citations


Respiratory syncytial virus (RSV) infection is a leading cause of severe lower respiratory tract illness in young infants, the elderly and immunocompromised individuals. We demonstrate here that the co-inhibitory molecule programmed cell death 1 (PD-1) is selectively upregulated on T cells within the respiratory tract during both murine and human RSV infection. Importantly, the interaction of PD-1 with its ligand PD-L1 is vital to restrict the pro-inflammatory activities of lung effector T cells in situ, thereby inhibiting the development of excessive pulmonary inflammation and injury during RSV infection. We further identify that PD-L1 expression on lung inflammatory dendritic cells is critical to suppress inflammatory T-cell activities, and an interferon-STAT1-IRF1 axis is responsible for increased PD-L1 expression on lung inflammatory dendritic cells. Our findings suggest a potentially critical role of PD-L1 and PD-1 interactions in the lung for controlling host inflammatory responses and disease progression in clinical RSV infection.

Original languageEnglish (US)
Pages (from-to)746-759
Number of pages14
JournalMucosal Immunology
Issue number4
StatePublished - Jul 25 2015


ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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