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| Content Provider | PubMed Central |
|---|---|
| Author | Elena, Sandalova Wei, Cheng-hong Masucci, Maria G. Levitsky, Victor |
| Copyright Year | 2004 |
| Abstract | Bim, a proapoptotic BH3-only member of the Bcl-2 protein family, is required for central and peripheral deletion of T lymphocytes. Mechanisms regulating Bim activity in T cells remain poorly understood. We show that expression of Bim is up-regulated in human T cells after polyclonal or specific T cell receptor triggering. Induction of Bim was affected by the agonistic potency of MHC:peptide ligands. Peptides that failed to induce Bim expression, failed to induce apoptosis in specific T cells, whereas partially agonistic ligands, which trigger death receptor-independent activation-induced cell death (AICD), induced Bim, but were inefficient in up-regulating Bcl-XL. Activation of protein kinase C and calcineurin appeared to be necessary and sufficient for Bim up-regulation after T cell receptor ligation. Immunosuppressive drugs known to prevent T cell deletion in vivo, such as cyclosporin A or FK506, blocked Bim up-regulation and rescued T cells from death receptor-independent AICD, whereas rapamycin, which allows the development of stable immunological tolerance, did not exhibit these activities. These results define a new mode of Bim regulation, strongly implicate Bim as a mediator of AICD, and suggest that Bim up-regulation can be targeted to influence the outcome of specific immune responses. |
| Related Links | http://dx.doi.org/10.1073/pnas.0400005101 |
| Ending Page | 3016 |
| Page Count | 6 |
| Starting Page | 3011 |
| File Format | |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 9 |
| Volume Number | 101 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2004-03-02 |
| Access Restriction | Open |
| Rights Holder | National Academy of Sciences |
| Subject Keyword | General Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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