Bcl-XL displays restricted distribution during T cell development and inhibits multiple forms of apoptosis but not clonal deletion in transgenic mice.
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- D A Grillot
- Department of Pathology, University of Michigan, Ann Arbor 48109-0608, USA.
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- R Merino
- Department of Pathology, University of Michigan, Ann Arbor 48109-0608, USA.
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- G Núñez
- Department of Pathology, University of Michigan, Ann Arbor 48109-0608, USA.
抄録
<jats:p>The survival of T lymphocytes is tightly controlled during development. Here, we show that Bcl-xL, a protein homologue of Bcl-2, is highly regulated in the thymus in a pattern different than that of Bcl-2. The maximum expression was in CD4+CD8+ thymocytes, a developmental stage where Bcl-2 is downregulated. To assess the role of Bcl-xL in thymocyte apoptosis, we generated mice overexpressing an E mu-bcl-x transgene within the T cell compartment. Constitutive expression of Bcl-xL resulted in accumulation of thymocytes and mature T cells in lymphoid organs. Thymocytes overexpressing Bcl-xL exhibited increased viability in vitro and were resistant to apoptosis induced by different signals, including glucocorticoid, gamma irradiation, calcium ionophore, and CD3 cross-linking. However, Bcl-xL was unable to block clonal deletion of thymocytes reactive with self-superantigens or H-Y antigen. These studies demonstrate that Bcl-2 and Bcl-xL, two functionally related proteins, are regulated independently during T cell development. In contrast to Bcl-2, which has been implicated in the maintenance of mature T cells, Bcl-xL appears to provide a survival signal for the maintenance of more immature CD4+CD8+ thymocytes before positive selection.</jats:p>
収録刊行物
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- The Journal of experimental medicine
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The Journal of experimental medicine 182 (6), 1973-1983, 1995-12-01
Rockefeller University Press
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詳細情報 詳細情報について
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- CRID
- 1361981471455473664
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- NII論文ID
- 30017433048
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- ISSN
- 15409538
- 00221007
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- データソース種別
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