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  • The TACI Receptor Regulates T-Cell-Independent Marginal Zone B Cell Responses through Innate Activation-Induced Cell Death

    Author(s)
    A. Figgett, William
    Fairfax, Kirsten
    B. Vincent, Fabien
    A. Le Page, Mélanie
    Katik, Indzi
    Deliyanti, Devy
    Quah, Pin Shie
    Verma, Pali
    Grumont, Raelene
    Gerondakis, Steve
    Hertzog, Paul
    A. O⿿Reilly, Lorraine
    Strasser, Andreas
    Mackay, Fabienne
    Griffith University Author(s)
    Verma, Pali
    Year published
    2013
    Metadata
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    Abstract
    Activation-induced cell death (AICD) plays a critical role in immune homeostasis and tolerance. In T-cell-dependent humoral responses, AICD of B cells is initiated by Fas ligand (FasL) on T cells, stimulating the Fas receptor on B cells. In contrast, T-cell-independent B cell responses involve innate-type B lymphocytes, such as marginal zone (MZ) B cells, and little is known about the mechanisms that control AICD during innate B cell responses to Toll-like receptor (TLR) activation. Here, we show that MZ B cells undergo AICD in response to TLR4 activation in vivo. The transmembrane activator, calcium modulator, and cyclophilin ...
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    Activation-induced cell death (AICD) plays a critical role in immune homeostasis and tolerance. In T-cell-dependent humoral responses, AICD of B cells is initiated by Fas ligand (FasL) on T cells, stimulating the Fas receptor on B cells. In contrast, T-cell-independent B cell responses involve innate-type B lymphocytes, such as marginal zone (MZ) B cells, and little is known about the mechanisms that control AICD during innate B cell responses to Toll-like receptor (TLR) activation. Here, we show that MZ B cells undergo AICD in response to TLR4 activation in vivo. The transmembrane activator, calcium modulator, and cyclophilin ligand interactor (TACI) receptor and TLR4 cooperate to upregulate expression of both FasL and Fas on MZ B cells and also to repress inhibitors of Fas-induced apoptosis signaling. These findings demonstrate an unappreciated role for TACI and its ligands in the regulation of AICD during T-cell-independent B cell responses.
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    Journal Title
    Immunity
    Volume
    39
    Issue
    3
    DOI
    https://doi.org/10.1016/j.immuni.2013.05.019
    Subject
    Immunology not elsewhere classified
    Neurosciences not elsewhere classified
    Biological Sciences not elsewhere classified
    Immunology
    Publication URI
    http://hdl.handle.net/10072/60581
    Collection
    • Journal articles

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