Direct evidence that interferon-β mediates enhanced HLA-class I expression in measles virus-infected cells

S. S. Dhib-Jalbut, E. P. Cowan

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44 Scopus citations


Viral infection results in enhancement of HLA-class I expression in a number of cell types, including glial cells, which normally do not express these molecules. This enhancement may occur through a direct interaction between a viral component and the HLA-class I gene or indirectly through virus-induced soluble factors produced by infected cells. These include cytokines such as IFN-γ, IFN-α/β, and TNF-α, known to enhance class I expression. Measles virus (MV) infection of a human glioma cell line (U-105 MG) and of primary human umbilical vein endothelial cells enhances the expression of HLA-class I molecules on these cells. The enhancement of HLA- class I is dependent on infectious virus, as antibody-neutralized MV has no effect on class I expression. In this study, we demonstrate the presence of an HLA-class I-enhancing factor in supernatants from MV-infected cells. The supernatant class I-enhancing factor is not IFN-γ, IFN-α, or TNF-α because MV-infected cells did not produce measurable levels of these cytokines as detected by immunoassay or polymerase chain reaction. In contrast, IFN-β is produced by the infected cells and the supernatant class I-enhancing factor could be entirely neutralized by antibodies to IFN-β, but not antibodies to IFN-α, TNF-α, or non-immune sera. Furthermore, preincubation of cells with neutralizing antibodies to IFN-β prior to infection blocked MV enhancement of HLA-class I completely in the U-105 MG cells and by as much as 74% in the umbilical vein endothelial cells. The results of these experiments provide direct evidence that enhanced HLA-class I expression in MV-infected cells is mediated primarily by IFN-β.

Original languageEnglish (US)
Pages (from-to)6248-6258
Number of pages11
JournalJournal of Immunology
Issue number11
StatePublished - 1993
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology


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