he host immune response. For example, adenoviruses that infect humans (which most commonly cause respiratory infections) produce several proteins that enable the virus to escape immune responses mediated by the pro-inflammatory soluble factor TNF. One of these proteins, E3-14.7K, inhibits the ability of TNF to cause the virus-infected cell to die. But exactly how it inhibits this process was previously unknown. Now, Stefan Schtze and colleagues from University Hospital of Schleswig-Holstein, Germany, show that expression of E3-14.7K in both human and mouse cells inhibits the internalization of TNF receptor 1 (TNFR1). This in turn prevents TNFR1 recruiting the other proteins it needs to cause the cell to die. Similar retention of TNFR1 at the cell surface was observed in human cells infected with E3-14.7K-expressing adenovirus. This study, which appears online on October 5 in advance of publication in the November print issue of the Journal of Clinical Investigation, describes a new mechanism of viral evasion of the immune response.
TITLE: Inhibition of TNF receptor 1 internalization by adenovirus 14.7K as a novel immune escape mechanism
University Hospital of Schleswig-Holstein, Kiel, Germany.
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View the PDF of this article at: https://www.the-jci.org/article.php?id=23771
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