The interferon-related developmental regulator 1 is used by human papillomavirus to suppress NFκB activation

Bart Tummers, Renske Goedemans, Laetitia P. L. Pelascini, Ekaterina S. Jordanova, Edith M. G. van Esch, Craig Meyers, Cornelis J. M. Melief, Judith M. Boer and Sjoerd H. van der Burg ()
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Bart Tummers: Leiden University Medical Center
Renske Goedemans: Leiden University Medical Center
Laetitia P. L. Pelascini: Leiden University Medical Center
Ekaterina S. Jordanova: Center for Gynaecological Oncology
Edith M. G. van Esch: Leiden University Medical Center
Craig Meyers: The Pennsylvania State University College of Medicine
Cornelis J. M. Melief: Leiden University Medical Center
Judith M. Boer: Leiden University Medical Center
Sjoerd H. van der Burg: Leiden University Medical Center

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract High-risk human papillomaviruses (hrHPVs) infect keratinocytes and successfully evade host immunity despite the fact that keratinocytes are well equipped to respond to innate and adaptive immune signals. Using non-infected and freshly established or persistent hrHPV-infected keratinocytes we show that hrHPV impairs the acetylation of NFκB/RelA K310 in keratinocytes. As a consequence, keratinocytes display a decreased pro-inflammatory cytokine production and immune cell attraction in response to stimuli of the innate or adaptive immune pathways. HPV accomplishes this by augmenting the expression of interferon-related developmental regulator 1 (IFRD1) in an EGFR-dependent manner. Restoration of NFκB/RelA acetylation by IFRD1 shRNA, cetuximab treatment or the HDAC1/3 inhibitor entinostat increases basal and induced cytokine expression. Similar observations are made in IFRD1-overexpressing HPV-induced cancer cells. Thus, our study reveals an EGFR–IFRD1-mediated viral immune evasion mechanism, which can also be exploited by cancer cells.

Date: 2015
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DOI: 10.1038/ncomms7537

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