Respiratory Syncytial Virus Infection of Human Respiratory Epithelial Cells Up-Regulates Class I MHC Expression Through the Induction of IFN-β and IL-1β

Roberto Garofalo, Fang Mei, Rosario Espejo, Gang Ye, Helene Haeberle, Samuel Baron, Pearay L. Ogra, Victor Reyes

Research output: Contribution to journalArticle

82 Citations (Scopus)

Abstract

CD8+ T cells mediate some of the damage to the lung epithelium following respiratory syncytial virus (RSV) infection. Since CD8+ T cells recognize antigen-laden class I MHC molecules on the target cells, we examined in this study the expression of class I MHC by RSV-infected respiratory epithelial cells. Respiratory epithelial cell lines and bronchial epithelial cells from normal human tissue responded to RSV infection with an increased expression of class I MHC as determined by flow cytometry and immunoprecipitation of class I MHC from metabolically radiolabeled cells. The increase in class I MHC expression was dependent on infectious, replicating virus. UV-irradiated culture supernatants from RSV-infected A549 cells, when added to fresh A549 cell cultures, induced an increase in class I MHC expression by those cells. The class I MHC increasing activity within supernatants from A549 cells was due, in large part, to IFN-β, and to a lesser extent to IL-1α. The addition of neutralizing Abs to both cytokines completely blocked the increase in class I MHC expression by cells treated with the above-mentioned supernatants. These results demonstrate that RSV infection elicits IFN-β production by respiratory epithelial cells, which in turn leads to an increase in their synthesis of class I MHC, which would facilitate their recognition and lysis by RSV-specific CD8+ T cells.

Original languageEnglish (US)
Pages (from-to)2506-2513
Number of pages8
JournalJournal of Immunology
Volume157
Issue number6
StatePublished - Sep 15 1996

Fingerprint

Respiratory Syncytial Virus Infections
Interleukin-1
Respiratory Syncytial Viruses
Up-Regulation
Epithelial Cells
T-Lymphocytes
Histocompatibility Antigens Class I
Immunoprecipitation
Flow Cytometry
Epithelium
Cell Culture Techniques
Cytokines
Viruses
Cell Line
Lung
A549 Cells

ASJC Scopus subject areas

  • Immunology

Cite this

Respiratory Syncytial Virus Infection of Human Respiratory Epithelial Cells Up-Regulates Class I MHC Expression Through the Induction of IFN-β and IL-1β. / Garofalo, Roberto; Mei, Fang; Espejo, Rosario; Ye, Gang; Haeberle, Helene; Baron, Samuel; Ogra, Pearay L.; Reyes, Victor.

In: Journal of Immunology, Vol. 157, No. 6, 15.09.1996, p. 2506-2513.

Research output: Contribution to journalArticle

Garofalo, Roberto ; Mei, Fang ; Espejo, Rosario ; Ye, Gang ; Haeberle, Helene ; Baron, Samuel ; Ogra, Pearay L. ; Reyes, Victor. / Respiratory Syncytial Virus Infection of Human Respiratory Epithelial Cells Up-Regulates Class I MHC Expression Through the Induction of IFN-β and IL-1β. In: Journal of Immunology. 1996 ; Vol. 157, No. 6. pp. 2506-2513.
@article{108477ebc31e413386b8cfad9d6e7907,
title = "Respiratory Syncytial Virus Infection of Human Respiratory Epithelial Cells Up-Regulates Class I MHC Expression Through the Induction of IFN-β and IL-1β",
abstract = "CD8+ T cells mediate some of the damage to the lung epithelium following respiratory syncytial virus (RSV) infection. Since CD8+ T cells recognize antigen-laden class I MHC molecules on the target cells, we examined in this study the expression of class I MHC by RSV-infected respiratory epithelial cells. Respiratory epithelial cell lines and bronchial epithelial cells from normal human tissue responded to RSV infection with an increased expression of class I MHC as determined by flow cytometry and immunoprecipitation of class I MHC from metabolically radiolabeled cells. The increase in class I MHC expression was dependent on infectious, replicating virus. UV-irradiated culture supernatants from RSV-infected A549 cells, when added to fresh A549 cell cultures, induced an increase in class I MHC expression by those cells. The class I MHC increasing activity within supernatants from A549 cells was due, in large part, to IFN-β, and to a lesser extent to IL-1α. The addition of neutralizing Abs to both cytokines completely blocked the increase in class I MHC expression by cells treated with the above-mentioned supernatants. These results demonstrate that RSV infection elicits IFN-β production by respiratory epithelial cells, which in turn leads to an increase in their synthesis of class I MHC, which would facilitate their recognition and lysis by RSV-specific CD8+ T cells.",
author = "Roberto Garofalo and Fang Mei and Rosario Espejo and Gang Ye and Helene Haeberle and Samuel Baron and Ogra, {Pearay L.} and Victor Reyes",
year = "1996",
month = "9",
day = "15",
language = "English (US)",
volume = "157",
pages = "2506--2513",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "6",

}

TY - JOUR

T1 - Respiratory Syncytial Virus Infection of Human Respiratory Epithelial Cells Up-Regulates Class I MHC Expression Through the Induction of IFN-β and IL-1β

AU - Garofalo, Roberto

AU - Mei, Fang

AU - Espejo, Rosario

AU - Ye, Gang

AU - Haeberle, Helene

AU - Baron, Samuel

AU - Ogra, Pearay L.

AU - Reyes, Victor

PY - 1996/9/15

Y1 - 1996/9/15

N2 - CD8+ T cells mediate some of the damage to the lung epithelium following respiratory syncytial virus (RSV) infection. Since CD8+ T cells recognize antigen-laden class I MHC molecules on the target cells, we examined in this study the expression of class I MHC by RSV-infected respiratory epithelial cells. Respiratory epithelial cell lines and bronchial epithelial cells from normal human tissue responded to RSV infection with an increased expression of class I MHC as determined by flow cytometry and immunoprecipitation of class I MHC from metabolically radiolabeled cells. The increase in class I MHC expression was dependent on infectious, replicating virus. UV-irradiated culture supernatants from RSV-infected A549 cells, when added to fresh A549 cell cultures, induced an increase in class I MHC expression by those cells. The class I MHC increasing activity within supernatants from A549 cells was due, in large part, to IFN-β, and to a lesser extent to IL-1α. The addition of neutralizing Abs to both cytokines completely blocked the increase in class I MHC expression by cells treated with the above-mentioned supernatants. These results demonstrate that RSV infection elicits IFN-β production by respiratory epithelial cells, which in turn leads to an increase in their synthesis of class I MHC, which would facilitate their recognition and lysis by RSV-specific CD8+ T cells.

AB - CD8+ T cells mediate some of the damage to the lung epithelium following respiratory syncytial virus (RSV) infection. Since CD8+ T cells recognize antigen-laden class I MHC molecules on the target cells, we examined in this study the expression of class I MHC by RSV-infected respiratory epithelial cells. Respiratory epithelial cell lines and bronchial epithelial cells from normal human tissue responded to RSV infection with an increased expression of class I MHC as determined by flow cytometry and immunoprecipitation of class I MHC from metabolically radiolabeled cells. The increase in class I MHC expression was dependent on infectious, replicating virus. UV-irradiated culture supernatants from RSV-infected A549 cells, when added to fresh A549 cell cultures, induced an increase in class I MHC expression by those cells. The class I MHC increasing activity within supernatants from A549 cells was due, in large part, to IFN-β, and to a lesser extent to IL-1α. The addition of neutralizing Abs to both cytokines completely blocked the increase in class I MHC expression by cells treated with the above-mentioned supernatants. These results demonstrate that RSV infection elicits IFN-β production by respiratory epithelial cells, which in turn leads to an increase in their synthesis of class I MHC, which would facilitate their recognition and lysis by RSV-specific CD8+ T cells.

UR - http://www.scopus.com/inward/record.url?scp=0030587083&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030587083&partnerID=8YFLogxK

M3 - Article

C2 - 8805651

AN - SCOPUS:0030587083

VL - 157

SP - 2506

EP - 2513

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 6

ER -