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    Maturation of marginal zone and follicular B cells requires B cell activating factor of the tumor necrosis factor family and is independent of B cell maturation antigen

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    Author
    Schneider, P; Takatsuka, H; Wilson, A; Mackay, F; Tardivel, A; Lens, S; Cachero, TG; Finke, D; Beermann, F; Tschopp, J
    Date
    2001-12-03
    Source Title
    Journal of Experimental Medicine
    Publisher
    ROCKEFELLER UNIV PRESS
    University of Melbourne Author/s
    Mackay, Fabienne
    Affiliation
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Schneider, P., Takatsuka, H., Wilson, A., Mackay, F., Tardivel, A., Lens, S., Cachero, T. G., Finke, D., Beermann, F. & Tschopp, J. (2001). Maturation of marginal zone and follicular B cells requires B cell activating factor of the tumor necrosis factor family and is independent of B cell maturation antigen. JOURNAL OF EXPERIMENTAL MEDICINE, 194 (11), pp.1691-1697. https://doi.org/10.1084/jem.194.11.1691.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257073
    DOI
    10.1084/jem.194.11.1691
    Abstract
    B cells undergo a complex series of maturation and selection steps in the bone marrow and spleen during differentiation into mature immune effector cells. The tumor necrosis factor (TNF) family member B cell activating factor of the TNF family (BAFF) (BLyS/TALL-1) plays an important role in B cell homeostasis. BAFF and its close homologue a proliferation-inducing ligand (APRIL) have both been shown to interact with at least two receptors, B cell maturation antigen (BCMA) and transmembrane activator and cyclophilin ligand interactor (TACI), however their relative contribution in transducing BAFF signals in vivo remains unclear. To functionally inactivate both BAFF and APRIL, mice transgenic for a soluble form of TACI were generated. They display a developmental block of B cell maturation in the periphery, leading to a severe depletion of marginal zone and follicular B2 B cells, but not of peritoneal B1 B cells. In contrast, mice transgenic for a soluble form of BCMA, which binds APRIL, have no detectable B cell phenotype. This demonstrates a crucial role for BAFF in B cell maturation and strongly suggests that it signals via a BCMA-independent pathway and in an APRIL-dispensable way.

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