Intravenous injection of soluble antigen induces thymic and peripheral T-cells apoptosis.
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- R S Liblau
- Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA.
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- R Tisch
- Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA.
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- K Shokat
- Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA.
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- X Yang
- Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA.
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- N Dumont
- Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA.
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- C C Goodnow
- Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA.
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- H O McDevitt
- Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA.
説明
<jats:p>The mechanism by which tolerance is induced via systemic administration of high doses of aqueous antigen has been analyzed by using mice transgenic for a T-cell receptor specific for the influenza virus hemagglutinin (HA) peptide comprising amino acids 126-138. After intravenous injection of 750 (but not 75) micrograms of HA peptide, a state of hyporesponsiveness was rapidly induced. In the thymus, in situ apoptosis in the cortex and at the corticomedullary junction was responsible for a synchronous and massive deletion of CD4+ CD8+ thymocytes. In secondary lymphoid organs, HA-reactive T cells were initially activated but were hyporesponsive at the single cell level. After 3 days, however, those cells were rapidly deleted, at least partially, through an apoptotic process. Therefore, both thymic and peripheral apoptosis, in addition to T-cell receptor desensitization, contribute to high-dose tolerance.</jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 93 (7), 3031-3036, 1996-04-02
Proceedings of the National Academy of Sciences
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詳細情報 詳細情報について
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- CRID
- 1362825895612478208
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- NII論文ID
- 30016219953
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- ISSN
- 10916490
- 00278424
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- データソース種別
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