Pulmonary immunity to viral infection: Adenoviras infection of lung dendritic cells renders T cells nonresponsive to interleukin-2

Allison T. Thiele, Tina L. Sumpter, Joanna A. Walker, Qi Xu, Cheong Hee Chang, Robert L. Bacallao, Rajesh Kher, David S. Wilkes

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Adenovirus (Ad) infection has been identified as predisposing hosts to the development of pulmonary disease through unknown mechanisms. Lung dendritic cells (DCs) are vital for initiating pulmonary immune responses; however, the effects of Ad infection on primary lung DC have not been studied. In contrast to the effects on bone marrow- and monocyte-derived DCs, the current study shows that Ad infection of marine BALB/c lung DCs in vitro and in vivo suppresses DC-induced T-cell proliferation. The effect of Ad on DCs was not due to a downregulation of major histocompatibility complex or costimulatory molecules. Analysis of the production of interleukin-12 (IL-12), alpha interferon (IFN-α), and IFN-γ by the Ad-infected DCs shows no significant differences over noninfected control lung DCs. Ad-induced suppression was not due to a deficiency of IL-2 or other DC-secreted factors and was dependent on viral protein synthesis, as UV irradiation of Ad abrogated the suppressive effect. Results suggest that Ad-infected DCs induce T cells to be nonresponsive to IL-2 during primary coculture, as the addition of IL-2 in secondary cultures recovered T-cell proliferation. In vivo studies supported in vitro results showing that Ad infection resulted in lung T cells with decreased proliferative ability. This study demonstrates that Ad infection induces local immunoincompetence by altering DC-T-cell interactions.

Original languageEnglish (US)
Pages (from-to)1826-1836
Number of pages11
JournalJournal of virology
Volume80
Issue number4
DOIs
StatePublished - Feb 1 2006

Fingerprint

Virus Diseases
dendritic cells
interleukin-2
Dendritic Cells
Interleukin-2
Immunity
T-lymphocytes
immunity
lungs
T-Lymphocytes
Lung
Adenoviridae Infections
Infection
Adenoviridae
infection
cell proliferation
Cell Proliferation
interferon-alpha
viral proteins
interleukin-12

ASJC Scopus subject areas

  • Microbiology
  • Immunology
  • Insect Science
  • Virology

Cite this

Pulmonary immunity to viral infection : Adenoviras infection of lung dendritic cells renders T cells nonresponsive to interleukin-2. / Thiele, Allison T.; Sumpter, Tina L.; Walker, Joanna A.; Xu, Qi; Chang, Cheong Hee; Bacallao, Robert L.; Kher, Rajesh; Wilkes, David S.

In: Journal of virology, Vol. 80, No. 4, 01.02.2006, p. 1826-1836.

Research output: Contribution to journalArticle

Thiele, Allison T. ; Sumpter, Tina L. ; Walker, Joanna A. ; Xu, Qi ; Chang, Cheong Hee ; Bacallao, Robert L. ; Kher, Rajesh ; Wilkes, David S. / Pulmonary immunity to viral infection : Adenoviras infection of lung dendritic cells renders T cells nonresponsive to interleukin-2. In: Journal of virology. 2006 ; Vol. 80, No. 4. pp. 1826-1836.
@article{8b1a8d8260d14a53a4bb5c57ba4ec5f1,
title = "Pulmonary immunity to viral infection: Adenoviras infection of lung dendritic cells renders T cells nonresponsive to interleukin-2",
abstract = "Adenovirus (Ad) infection has been identified as predisposing hosts to the development of pulmonary disease through unknown mechanisms. Lung dendritic cells (DCs) are vital for initiating pulmonary immune responses; however, the effects of Ad infection on primary lung DC have not been studied. In contrast to the effects on bone marrow- and monocyte-derived DCs, the current study shows that Ad infection of marine BALB/c lung DCs in vitro and in vivo suppresses DC-induced T-cell proliferation. The effect of Ad on DCs was not due to a downregulation of major histocompatibility complex or costimulatory molecules. Analysis of the production of interleukin-12 (IL-12), alpha interferon (IFN-α), and IFN-γ by the Ad-infected DCs shows no significant differences over noninfected control lung DCs. Ad-induced suppression was not due to a deficiency of IL-2 or other DC-secreted factors and was dependent on viral protein synthesis, as UV irradiation of Ad abrogated the suppressive effect. Results suggest that Ad-infected DCs induce T cells to be nonresponsive to IL-2 during primary coculture, as the addition of IL-2 in secondary cultures recovered T-cell proliferation. In vivo studies supported in vitro results showing that Ad infection resulted in lung T cells with decreased proliferative ability. This study demonstrates that Ad infection induces local immunoincompetence by altering DC-T-cell interactions.",
author = "Thiele, {Allison T.} and Sumpter, {Tina L.} and Walker, {Joanna A.} and Qi Xu and Chang, {Cheong Hee} and Bacallao, {Robert L.} and Rajesh Kher and Wilkes, {David S.}",
year = "2006",
month = "2",
day = "1",
doi = "10.1128/JVI.80.4.1826-1836.2006",
language = "English (US)",
volume = "80",
pages = "1826--1836",
journal = "Journal of Virology",
issn = "0022-538X",
publisher = "American Society for Microbiology",
number = "4",

}

TY - JOUR

T1 - Pulmonary immunity to viral infection

T2 - Adenoviras infection of lung dendritic cells renders T cells nonresponsive to interleukin-2

AU - Thiele, Allison T.

AU - Sumpter, Tina L.

AU - Walker, Joanna A.

AU - Xu, Qi

AU - Chang, Cheong Hee

AU - Bacallao, Robert L.

AU - Kher, Rajesh

AU - Wilkes, David S.

PY - 2006/2/1

Y1 - 2006/2/1

N2 - Adenovirus (Ad) infection has been identified as predisposing hosts to the development of pulmonary disease through unknown mechanisms. Lung dendritic cells (DCs) are vital for initiating pulmonary immune responses; however, the effects of Ad infection on primary lung DC have not been studied. In contrast to the effects on bone marrow- and monocyte-derived DCs, the current study shows that Ad infection of marine BALB/c lung DCs in vitro and in vivo suppresses DC-induced T-cell proliferation. The effect of Ad on DCs was not due to a downregulation of major histocompatibility complex or costimulatory molecules. Analysis of the production of interleukin-12 (IL-12), alpha interferon (IFN-α), and IFN-γ by the Ad-infected DCs shows no significant differences over noninfected control lung DCs. Ad-induced suppression was not due to a deficiency of IL-2 or other DC-secreted factors and was dependent on viral protein synthesis, as UV irradiation of Ad abrogated the suppressive effect. Results suggest that Ad-infected DCs induce T cells to be nonresponsive to IL-2 during primary coculture, as the addition of IL-2 in secondary cultures recovered T-cell proliferation. In vivo studies supported in vitro results showing that Ad infection resulted in lung T cells with decreased proliferative ability. This study demonstrates that Ad infection induces local immunoincompetence by altering DC-T-cell interactions.

AB - Adenovirus (Ad) infection has been identified as predisposing hosts to the development of pulmonary disease through unknown mechanisms. Lung dendritic cells (DCs) are vital for initiating pulmonary immune responses; however, the effects of Ad infection on primary lung DC have not been studied. In contrast to the effects on bone marrow- and monocyte-derived DCs, the current study shows that Ad infection of marine BALB/c lung DCs in vitro and in vivo suppresses DC-induced T-cell proliferation. The effect of Ad on DCs was not due to a downregulation of major histocompatibility complex or costimulatory molecules. Analysis of the production of interleukin-12 (IL-12), alpha interferon (IFN-α), and IFN-γ by the Ad-infected DCs shows no significant differences over noninfected control lung DCs. Ad-induced suppression was not due to a deficiency of IL-2 or other DC-secreted factors and was dependent on viral protein synthesis, as UV irradiation of Ad abrogated the suppressive effect. Results suggest that Ad-infected DCs induce T cells to be nonresponsive to IL-2 during primary coculture, as the addition of IL-2 in secondary cultures recovered T-cell proliferation. In vivo studies supported in vitro results showing that Ad infection resulted in lung T cells with decreased proliferative ability. This study demonstrates that Ad infection induces local immunoincompetence by altering DC-T-cell interactions.

UR - http://www.scopus.com/inward/record.url?scp=32444436341&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=32444436341&partnerID=8YFLogxK

U2 - 10.1128/JVI.80.4.1826-1836.2006

DO - 10.1128/JVI.80.4.1826-1836.2006

M3 - Article

C2 - 16439539

AN - SCOPUS:32444436341

VL - 80

SP - 1826

EP - 1836

JO - Journal of Virology

JF - Journal of Virology

SN - 0022-538X

IS - 4

ER -