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, Baohua Zhou, Stephanie Davis, N. L. Krupp, T. J. Braciale, Jie Sun

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

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
Volume8
Issue number4
DOIs
StatePublished - Jul 25 2015

Fingerprint

Respiratory Syncytial Virus Infections
Dendritic Cells
T-Lymphocytes
Lung
Cell Death
Respiratory System
Human respiratory syncytial virus
Lung Injury
Interferons
Disease Progression
Pneumonia
Ligands

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Control of pathogenic effector T-cell activities in situ by PD-L1 expression on respiratory inflammatory dendritic cells during respiratory syncytial virus infection. / Yao, S.; Jiang, L.; Moser, E. K.; Jewett, L. B.; Wright, J.; Du, J.; Zhou, Baohua; Davis, Stephanie; Krupp, N. L.; Braciale, T. J.; Sun, Jie.

In: Mucosal Immunology, Vol. 8, No. 4, 25.07.2015, p. 746-759.

Research output: Contribution to journalArticle

@article{4691d453955443ce9135aa5d8770ed05,
title = "Control of pathogenic effector T-cell activities in situ by PD-L1 expression on respiratory inflammatory dendritic cells during respiratory syncytial virus infection",
abstract = "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.",
author = "S. Yao and L. Jiang and Moser, {E. K.} and Jewett, {L. B.} and J. Wright and J. Du and Baohua Zhou and Stephanie Davis and Krupp, {N. L.} and Braciale, {T. J.} and Jie Sun",
year = "2015",
month = "7",
day = "25",
doi = "10.1038/mi.2014.106",
language = "English (US)",
volume = "8",
pages = "746--759",
journal = "Mucosal Immunology",
issn = "1933-0219",
publisher = "Nature Publishing Group",
number = "4",

}

TY - JOUR

T1 - Control of pathogenic effector T-cell activities in situ by PD-L1 expression on respiratory inflammatory dendritic cells during respiratory syncytial virus infection

AU - Yao, S.

AU - Jiang, L.

AU - Moser, E. K.

AU - Jewett, L. B.

AU - Wright, J.

AU - Du, J.

AU - Zhou, Baohua

AU - Davis, Stephanie

AU - Krupp, N. L.

AU - Braciale, T. J.

AU - Sun, Jie

PY - 2015/7/25

Y1 - 2015/7/25

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84932628981&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84932628981&partnerID=8YFLogxK

U2 - 10.1038/mi.2014.106

DO - 10.1038/mi.2014.106

M3 - Article

VL - 8

SP - 746

EP - 759

JO - Mucosal Immunology

JF - Mucosal Immunology

SN - 1933-0219

IS - 4

ER -