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• W2167787789 abstract "The antiapoptotic protein cellular FLICE (Fas-associated death domain-like IL-1beta-converting enzyme) inhibitory protein (cFLIP) protects cells from CD95(APO-1/Fas)-induced apoptosis in vitro and was found to be overexpressed in human melanomas. However, cytotoxic T cell-induced apoptosis, which is critically involved in tumor control in vivo, is not inhibited by cFLIP in vitro, as only CD95- and not perforin-dependent lysis is affected. This calls into question whether cFLIP is sufficient to allow escape from T cell-dependent immunity. Using two murine tumors, we directly demonstrate that cFLIP does result in escape from T cell immunity in vivo. Moreover, tumor cells are selected in vivo for elevated cFLIP expression. Therefore, our data indicate that CD95-dependent apoptosis constitutes a more prominent mechanism for tumor clearance than has so far been anticipated and that blockade of this pathway can result in tumor escape even when the perforin pathway is operational." @default.
• W2167787789 created "2016-06-24" @default.
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• W2167787789 date "1999-10-04" @default.
• W2167787789 modified "2023-10-18" @default.
• W2167787789 title "Immune Escape of Tumors in Vivo by Expression of Cellular Flice-Inhibitory Protein" @default.
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• W2167787789 doi "https://doi.org/10.1084/jem.190.7.1033" @default.
• W2167787789 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2195655" @default.
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