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Regulation of expression of Bcl-2 protein family member Bim by T cell receptor triggering.

Identifieur interne : 001877 ( Main/Exploration ); précédent : 001876; suivant : 001878

Regulation of expression of Bcl-2 protein family member Bim by T cell receptor triggering.

Auteurs : Elena Sandalova [Suède] ; Cheng-Hong Wei ; Maria G. Masucci ; Victor Levitsky

Source :

RBID : pubmed:14970329

Descripteurs français

English descriptors

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-X(L). 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.

DOI: 10.1073/pnas.0400005101
PubMed: 14970329
PubMed Central: PMC365736


Affiliations:


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Le document en format XML

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<div type="abstract" xml:lang="en">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-X(L). 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.</div>
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<ReferenceList>
<Reference>
<Citation>Nat Med. 1999 Nov;5(11):1303-7</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10545998</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Immunol. 1999 Sep 1;163(5):2601-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10452999</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Eur J Immunol. 2000 Feb;30(2):678-82</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10671226</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Eur J Immunol. 2000 Feb;30(2):683-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10671227</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Transplantation. 2000 Jun 15;69(11):2428-32</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10868653</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Biochem Biophys Res Commun. 2000 Jul 5;273(2):736-44</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10873673</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Am J Pathol. 2000 Aug;157(2):449-61</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10934149</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Biochem Soc Symp. 1999;66:1-15</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10989652</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Curr Biol. 2000 Oct 5;10(19):1201-4</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11050388</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Immunol. 2001 Jan 15;166(2):989-95</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11145677</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Mol Cell Biol. 2001 Feb;21(3):854-64</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11154272</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Immunol. 2001 Feb 15;166(4):2311-6</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11160287</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Blood. 2001 Mar 15;97(6):1803-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11238123</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Neuron. 2001 Mar;29(3):615-28</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11301022</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Neuron. 2001 Mar;29(3):629-43</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11301023</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Immunity. 2001 Apr;14(4):407-16</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11336686</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Mol Cell. 2001 Sep;8(3):705-11</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11583631</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Biol Chem. 2001 Oct 12;276(41):37754-60</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11495903</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Heart Lung Transplant. 2001 Oct;20(10):1132-5</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11595570</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Cell Biol. 2002 Feb 4;156(3):531-42</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11815629</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Nature. 2002 Feb 21;415(6874):922-6</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11859372</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cell Death Differ. 2002 May;9(5):505-12</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11973609</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Curr Opin Immunol. 2002 Jun;14(3):354-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11973134</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Cell Biol. 2002 Apr 29;157(3):441-53</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11980919</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Immunol. 2002 May 15;168(10):5024-31</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">11994454</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Immunity. 2002 Jun;16(6):759-67</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12121658</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Curr Opin Immunol. 2002 Oct;14(5):592-600</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12183158</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Hum Immunol. 2002 Oct;63(10):821-33</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12368034</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Cell. 2002 Oct 4;111(1):51-62</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12372300</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Oncogene. 2003 Mar 6;22(9):1281-93</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12618753</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Immunol Rev. 2003 Jun;193:70-81</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12752672</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Nat Cell Biol. 2003 Aug;5(8):733-40</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">12844146</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Exp Med. 2003 Oct 6;198(7):1119-26</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">14517273</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Proc Natl Acad Sci U S A. 1993 Mar 15;90(6):2217-21</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">8384718</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Mol Cell Cardiol. 1993 Dec;25(12):1461-9</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">7512654</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Biochem J. 1994 Sep 1;302 ( Pt 2):321-4</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">7522435</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Exp Med. 1996 Sep 1;184(3):1155-60</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9064332</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>EMBO J. 1998 Jan 15;17(2):384-95</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9430630</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Immunol. 1998 Jul 15;161(2):594-601</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">9670932</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Mol Cell. 1999 Mar;3(3):287-96</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10198631</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Annu Rev Immunol. 1999;17:221-53</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10358758</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>J Immunol. 1999 Sep 1;163(5):2500-7</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10452986</ArticleId>
</ArticleIdList>
</Reference>
<Reference>
<Citation>Science. 1999 Nov 26;286(5445):1735-8</Citation>
<ArticleIdList>
<ArticleId IdType="pubmed">10576740</ArticleId>
</ArticleIdList>
</Reference>
</ReferenceList>
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