Immune Escape of Tumors In Vivo by Expression of Cellular FLICE-inhibitory Protein

doi:10.1084/jem.190.7.1033

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© The Rockefeller University Press, 0022-1007/1999/10/1033/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 7, October 4, 1999 1033-1038

Immune Escape of Tumors In Vivo by Expression of Cellular FLICE-inhibitory Protein

Jan Paul Medema^a, Joan de Jong^a, Thorbald van Hall^a, Cornelis J.M. Melief^a, and Rienk Offringa^a
^a Department of Immunohematology and Bloodbank, Leiden University Medical Center, 2333AA Leiden, The Netherlands

Correspondence to: Jan Paul Medema, Dept. of Immunohematology and Bloodbank, LUMC, Albinusdreef 2a, 2333AA Leiden, The Netherlands. Tel:31-71-52-63013 Fax:31-71-52-16751 E-mail:medema{at}mail.medfac.leidenuniv.nl.

The antiapoptotic protein cellular FLICE (Fas-associated deathdomain–like IL-1ß–converting enzyme) inhibitoryprotein (cFLIP) protects cells from CD95(APO-1/Fas)-inducedapoptosis in vitro and was found to be overexpressed in humanmelanomas. However, cytotoxic T cell–induced apoptosis,which is critically involved in tumor control in vivo, is notinhibited by cFLIP in vitro, as only CD95- and not perforin-dependentlysis is affected. This calls into question whether cFLIP issufficient to allow escape from T cell–dependent immunity.Using two murine tumors, we directly demonstrate that cFLIPdoes 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 constitutesa more prominent mechanism for tumor clearance than has so farbeen anticipated and that blockade of this pathway can resultin tumor escape even when the perforin pathway is operational.

Key Words: CD95, apoptosis, CTL, perforin, cytotoxicity

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