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 language | English (US) |
|---|---|
| Pages (from-to) | 2506-2513 |
| Number of pages | 8 |
| Journal | Journal of Immunology |
| Volume | 157 |
| Issue number | 6 |
| State | Published - Sep 15 1996 |
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- 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 journal › Article
}
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.
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M3 - Article
VL - 157
SP - 2506
EP - 2513
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 6
ER -