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    Environmental sensing by mature B cells is controlled by the transcription factors PU.1 and SpiB

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    Author
    Willis, SN; Tellier, J; Liao, Y; Trezise, S; Light, A; O'Donnell, K; Garrett-Sinha, LA; Shi, W; Tarlinton, DM; Nutt, SL
    Date
    2017-11-10
    Source Title
    Nature Communications
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Shi, Wei; Willis, Simon; Tellier, Julie; Nutt, Stephen; Liao, Yang; Trezise, Stephanie
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Willis, S. N., Tellier, J., Liao, Y., Trezise, S., Light, A., O'Donnell, K., Garrett-Sinha, L. A., Shi, W., Tarlinton, D. M. & Nutt, S. L. (2017). Environmental sensing by mature B cells is controlled by the transcription factors PU.1 and SpiB. NATURE COMMUNICATIONS, 8 (1), https://doi.org/10.1038/s41467-017-01605-1.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257483
    DOI
    10.1038/s41467-017-01605-1
    Abstract
    Humoral immunity requires B cells to respond to multiple stimuli, including antigen, membrane and soluble ligands, and microbial products. Ets family transcription factors regulate many aspects of haematopoiesis, although their functions in humoral immunity are difficult to decipher as a result of redundancy between the family members. Here we show that mice lacking both PU.1 and SpiB in mature B cells do not generate germinal centers and high-affinity antibody after protein immunization. PU.1 and SpiB double-deficient B cells have a survival defect after engagement of CD40 or Toll-like receptors (TLR), despite paradoxically enhanced plasma cell differentiation. PU.1 and SpiB regulate the expression of many components of the B cell receptor signaling pathway and the receptors for CD40L, BAFF and TLR ligands. Thus, PU.1 and SpiB enable B cells to appropriately respond to environmental cues.

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