Normal Thymocyte Negative Selection in TRAIL-deficient Mice
Copyright policy )Normal Thymocyte Negative Selection in TRAIL-deficient Mice
The molecular basis of thymocyte negative selection, which plays a critical role in establishing and maintaining immunological tolerance, is not yet resolved. In particular, the importance of the death receptor subgroup of the tumor necrosis factor (TNF)-family has been the subject of many investigations, with equivocal results. A recent report suggested that TRAIL was a critical factor in this process, a result that does not fit well with previous studies that excluded a role for the FADD-caspase 8 pathway, which is essential for TRAIL and Fas ligand (FasL) signaling, in negative selection. We have investigated intrathymic negative selection of TRAIL-deficient thymocytes, using four well-established models, including antibody-mediated TCR/CD3 ligation in vitro, stimulation with endogenous superantigen in vitro and in vivo, and treatment with exogenous superantigen in vitro. We were unable to demonstrate a role for TRAIL signaling in any of these models, suggesting that this pathway is not a critical factor for thymocyte negative selection.
- University of Melbourne Australia
- Walter and Eliza Hall Institute of Medical Research Australia
- Monash University Australia
- Peter MacCallum Cancer Centre Australia
570, Mice, Inbred BALB C, Membrane Glycoproteins, Tumor Necrosis Factor-alpha, T-Lymphocytes, Brief Definitive Report, 610, Clonal Deletion, Mice, Inbred C57BL, TNF-Related Apoptosis-Inducing Ligand, Mice, Antigens, CD, Receptor-CD3 Complex, Antigen, T-Cell, T-Lymphocyte Subsets, Animals, Lymph Nodes, Apoptosis Regulatory Proteins, Gene Deletion, Spleen, Signal Transduction
570, Mice, Inbred BALB C, Membrane Glycoproteins, Tumor Necrosis Factor-alpha, T-Lymphocytes, Brief Definitive Report, 610, Clonal Deletion, Mice, Inbred C57BL, TNF-Related Apoptosis-Inducing Ligand, Mice, Antigens, CD, Receptor-CD3 Complex, Antigen, T-Cell, T-Lymphocyte Subsets, Animals, Lymph Nodes, Apoptosis Regulatory Proteins, Gene Deletion, Spleen, Signal Transduction
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