Objective Fas is a member of the TNF receptor family of proteins, that, when cross-linked by mAbs or its physiological ligand (FasL), induces apoptosis. Fas-mediated apoptosis is of physiological relevance in the regulation and function of the immune system. A biochemical mechanism for Fas-induced apoptosis, as well as for the apoptosis process itself, is unknown . Oxidative damage has been implicated in some forms of TNFmediated cytotoxicity. Mitochondrial respiration is the cellular process from which free radical could be more easily generated, and it is directly implicated in TNF-induced cell death of L929 cells. The implication of mitochondrial function in Fas-based cytotoxicity will be tested using mitochondrial DNA-depleted U937 and Jurkat cells, as both the promonocytic U937 and the T cell line Jurkat are sensitive to Fas-induced cytotoxicity. Fas-based cytotoxicity will be tested using effector T cells, that express the functional FasL on their surface upon activation, especially CD8+ CTL clones. Fields of science natural sciencesbiological sciencesbiochemistrybiomoleculesproteinsmedical and health sciencesbasic medicineimmunology Programme(s) FP4-TMR - Specific research and technological development programme in the field of the training and mobility of researchers, 1994-1998 Topic(s) 0302 - Post-doctoral research training grants TL07 - Immunology and Cancer Call for proposal Data not available Funding Scheme RGI - Research grants (individual fellowships) Coordinator Universidad de Zaragoza Address S/n,gomez laguna 50013 Zaragoza Spain See on map EU contribution € 0,00 Participants (1) Sort alphabetically Sort by EU Contribution Expand all Collapse all Not available Spain EU contribution € 0,00 Address See on map
