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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Immune escape of tumors in vivo by expression of cellular FLICE-inhibitory protein.

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.[1]

References

  1. Immune escape of tumors in vivo by expression of cellular FLICE-inhibitory protein. Medema, J.P., de Jong, J., van Hall, T., Melief, C.J., Offringa, R. J. Exp. Med. (1999) [Pubmed]
 
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