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Novel mechanism of immunosuppression by influenza virus haemagglutinin: selective suppression of interleukin 12 p35 transcription in murine bone marrow-derived dendritic cells

Noone, Cariosa M. and Lewis, Ellen A. and Frawely, Anne B. and Newman, Robert W. and Mahon, Bernard P. and Mills, Kingston H. and Johnson, Patricia A. (2005) Novel mechanism of immunosuppression by influenza virus haemagglutinin: selective suppression of interleukin 12 p35 transcription in murine bone marrow-derived dendritic cells. Journal of General Virology, 86. pp. 1885-1890.

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Abstract

Infection with influenza virus strongly predisposes an individual to bacterial superinfection, which is often the significant cause of morbidity and mortality during influenza epidemics. Little is known about the immunomodulating properties of the virus that lead to this phenomenon, but the effect of the viral components on the development of immune dendritic cells (DCs) may prove vital. In this study, activation of and cytokine secretion by bacterial lipopolysaccharide (LPS)-stimulated bone marrow-derived dendritic cells (BMDCs) following treatment with the influenza virus major antigen haemagglutinin (HA) were examined. HA selectively inhibits the release of LPS-induced interleukin 12 (IL12) p70, which is independent of IL10 secretion. Suppression occurs at the transcriptional level, with selective inhibition of p35- and not p40-subunit mRNA expression. The downregulation of IL12 p70 by influenza HA is a novel and unexplored pathway that may be relevant in the predisposition to bacterial superinfection associated with influenza virus infections.

Item Type: Article
Keywords: mechanism of immunosuppression; influenza virus; haemagglutinin; bone marrow-derived dendritic cells;
Subjects: Science & Engineering > Biology
Science & Engineering > Institute of Immunology
Item ID: 509
Depositing User: Dr. Bernard Mahon
Date Deposited: 03 May 2007
Journal or Publication Title: Journal of General Virology
Publisher: Society for General Microbiology
Refereed: Yes
URI:

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