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Regulatory T-cells limit acute but not memory T cell responses to acute viral infection.

Vortrag: 14th International Congress of Immunology, 22-27 August 2010, Kobe, Japan. (2010)
as soon as is submitted to ZB.
EBV-positive cells harbor an interferon inducing activity that is recognized by cellular receptors which are not yet identified. The potential candidates are the cytosolic RNA receptors namely the RIG-I-like receptors as well as the membrane anchored Toll-like receptors that recognize viral RNA or DNA, like TLR-3, -7, -8, -9. Any of these receptors might be activated by viral components leading to type I interferon response. However, in EBV-positive Burkitt lymphoma cells the type I interferon response and its signaling is impaired by deregulated high c-Myc expression due to a chromosomal translocation. Our model cell-line P493-6 expressing c-Myc in a tetracycline dependent fashion showed that interferon is produced and secreted 24-48h after switching off c-Myc expression. In this model system we’ve identified several interferon signaling components and cellular receptors which are suppressed by high expression of c-Myc. Thus c-MYC masks an interferon-inducing activity in these cells. This could be verified in Akata cells established from an EBV-positive Burkitt lymphoma by suppressing the c-Myc expression level. Our data provide evidence that c-Myc is the key transcriptional down-modulator of viral pattern recognition and interferon signaling in BL-cells implying that immune escape of tumor cells is not only a matter of in vivo selection but may be additionally promoted by activation of a cellular oncogene.
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Publication type Other: Lecture
Reviewing status