1. Defective thymocyte apoptosis and accelerated autoimmune diseases in TRAIL-/- mice.
- Author
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Lamhamedi-Cherradi SE, Zheng SJ, Maguschak KA, Peschon J, and Chen YH
- Subjects
- Animals, Apoptosis Regulatory Proteins, Autoimmune Diseases etiology, Autoimmune Diseases pathology, Cell Differentiation physiology, Clonal Deletion immunology, Collagen immunology, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Ovalbumin, T-Lymphocytes pathology, TNF-Related Apoptosis-Inducing Ligand, Thymus Gland immunology, Thymus Gland pathology, Apoptosis genetics, Autoimmune Diseases genetics, Membrane Glycoproteins genetics, T-Lymphocytes physiology, Tumor Necrosis Factor-alpha genetics
- 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.
- Published
- 2003
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