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    BH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytes

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    Author
    Bouillet, P; Purton, JF; Godfrey, DI; Zhang, LC; Coultas, L; Puthalakath, H; Pellegrini, M; Cory, S; Adams, JM; Strasser, A
    Date
    2002-02-21
    Source Title
    NATURE
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Godfrey, Dale; Cory, Suzanne; COULTAS, LEIGH; Bouillet, Philippe
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Bouillet, P., Purton, J. F., Godfrey, D. I., Zhang, L. C., Coultas, L., Puthalakath, H., Pellegrini, M., Cory, S., Adams, J. M. & Strasser, A. (2002). BH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytes. NATURE, 415 (6874), pp.922-926. https://doi.org/10.1038/415922a.
    Access Status
    This item is currently not available from this repository
    URI
    http://hdl.handle.net/11343/26373
    DOI
    10.1038/415922a
    Description

    C1 - Journal Articles Refereed

    Abstract
    During lymphocyte development, the assembly of genes coding for antigen receptors occurs by the combinatorial linking of gene segments. The stochastic nature of this process gives rise to lymphocytes that can recognize self-antigens, thereby having the potential to induce autoimmune disease. Such autoreactive lymphocytes can be silenced by developmental arrest or unresponsiveness (anergy), or can be deleted from the repertoire by cell death. In the thymus, developing T lymphocytes (thymocytes) bearing a T-cell receptor (TCR)-CD3 complex that engages self-antigens are induced to undergo programmed cell death (apoptosis), but the mechanisms ensuring this 'negative selection' are unclear. We now report that thymocytes lacking the pro-apoptotic Bcl-2 family member Bim (also known as Bcl2l11) are refractory to apoptosis induced by TCR-CD3 stimulation. Moreover, in transgenic mice expressing autoreactive TCRs that provoke widespread deletion, Bim deficiency severely impaired thymocyte killing. TCR ligation upregulated Bim expression and promoted interaction of Bim with Bcl-XL, inhibiting its survival function. These findings identify Bim as an essential initiator of apoptosis in thymocyte-negative selection.
    Keywords
    Cell Development (incl. Cell Division and Apoptosis) ; Genetic Immunology ; Cancer and Related Disorders

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