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Updated: Sep 20, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
Edmonston measles virus prevents increased cell surface expression of peptide-loaded major histocompatibility complex
Mamadi Yilla1, Carole Hickman, Marcia McGrew
1Respiratory and Enteric Viruses Branch, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA. mby7@cdc.gov
Abstract:
Gamma interferon (IFN-gamma) induces expression of the gene products of the major histocompatibility complex (MHC), whereas IFN-alpha/beta can interfere with or suppress class II protein expression. In separate studies, measles virus (MV) was reported to induce IFN-alpha/beta and to up-regulate MHC class II proteins. In an attempt to resolve this paradox, we examined the surface expression of MHC class I and class II proteins in MV-infected peripheral monocytes in the presence and absence of IFN-alpha/beta. Infection of purified monocytes with Edmonston B MV resulted in an apparent increase in cell surface expression of HLA-A, -B, and -C class I proteins, but it had no effect on the expression of HLA-DR class II proteins. MV-infected purified monocytes expressed IFN-alpha/beta, but no measurable IFN-gamma expression was detected in supernatant fluids. Class II protein expression could be enhanced by coculture of purified monocytes with uninfected peripheral blood mononuclear cell (PBMC) supernatant. MV infection of PBMCs also did not affect expression of class II proteins, but the expression of HLA-A, -B, and -C class I proteins was increased two- to threefold in most donor cells. A direct role for IFN-alpha/beta suppression of MHC class II protein expression was not evident in monocytes since MV suppressed class II protein expression in the absence of IFN-alpha/beta. Taken together, these data suggest that MV interferes with the expression of peptide-loaded class II complexes, an effect that may potentially alter CD4(+)-T-cell proliferation and the cell-mediated immune responses that they help to regulate.
Insights
Measles virus (MV) infection increases major histocompatibility complex (MHC) class I expression on monocytes but does not affect class II expression. MV interferes with peptide-loaded class II complexes, potentially altering T-cell responses.
Area of Science:
- Immunology
- Virology
Background:
- Interferon-gamma (IFN-γ) upregulates MHC expression, while Interferon-alpha/beta (IFN-α/β) can suppress MHC class II. Measles virus (MV) is known to induce IFN-α/β and has been reported to upregulate MHC class II.
- A paradox exists regarding MV's effect on MHC class II expression, as it induces IFN-α/β, which typically suppresses MHC class II.
Purpose of the Study:
- To investigate the surface expression of MHC class I and class II proteins in MV-infected peripheral monocytes.
- To resolve the apparent paradox of MV's influence on MHC class II expression in the presence and absence of IFN-α/β.
Main Methods:
- Purified monocytes were infected with Edmonston B MV.
- Surface expression of MHC class I (HLA-A, -B, -C) and class II (HLA-DR) proteins was analyzed.
- IFN-α/β and IFN-γ levels in supernatant fluids were measured.
- Monocytes were cocultured with peripheral blood mononuclear cell (PBMC) supernatant.
Main Results:
- MV infection of monocytes increased cell surface expression of MHC class I proteins but had no effect on MHC class II expression.
- MV-infected monocytes produced IFN-α/β, with no detectable IFN-γ.
- MV infection of PBMCs also increased MHC class I expression, without affecting MHC class II expression.
- MV suppressed class II protein expression independently of IFN-α/β presence.
Conclusions:
- MV interferes with the expression of peptide-loaded MHC class II complexes on monocytes.
- This interference may alter CD4(+) T-cell proliferation and regulate cell-mediated immune responses.
- The findings suggest a mechanism by which MV modulates the host immune system beyond the known effects of IFN-α/β.
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