Abstract
TRAIL, the tumor necrosis factor-related apoptosis-inducing ligand, selectively induces apoptosis of tumor cells, but not most normal cells. Its role in normal, nontransformed tissues is not clear. We report here that mice deficient in TRAIL have a severe defect in thymocyte apoptosis—thus, thymic deletion induced by T cell receptor ligation is severely impaired. TRAIL-deficient mice are also hypersensitive to collagen-induced arthritis and streptozotocin-induced diabetes and develop heightened autoimmune responses. Thus, TRAIL mediates thymocyte apoptosis and is important in the induction of autoimmune diseases.
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18 February 2003
spelling was corrected for online and print versions
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Acknowledgements
We thank J. Sun, E. Rowell, L.-Y. Xu, P. Wang and G. Tsabary for technical assistance, M. I. Greene and B. Hilliard for discussions. Supported by grants from the National Institutes of Health (AI50059, NS40188 and NS40447 to Y.H.C.).
*Note: In the version of this article initially published online, this paper contained a misspelling of the first author's name, which should have been spelled Salah-Eddine Lamhamedi-Cherradi. This mistake has been corrected in the HTML version and print versions of the article. We regret the error.
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Lamhamedi-Cherradi, SE., Zheng, SJ., Maguschak, K. et al. Defective thymocyte apoptosis and accelerated autoimmune diseases in TRAIL−/− mice. Nat Immunol 4, 255–260 (2003). https://doi.org/10.1038/ni894
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DOI: https://doi.org/10.1038/ni894
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