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    Hematopoiesis is finely regulated to enable timely production of the right numbers and types of mature immune cells to maintain tissue homeostasis. Dysregulated hematopoiesis may compromise antiviral immunity and/or exacerbate immunopathogenesis. Herein, we report an essential role of UBXN3B in maintenance of hematopoietic homeostasis and restriction of immunopathogenesis during respiratory viral infection. Ubxn3b deficient ( Ubxn3b -/- ) mice are highly vulnerable to SARS-CoV-2 and influenza A infection, characterized by more severe lung immunopathology, lower virus-specific IgG, significantly fewer B cells, but more myeloid cells than Ubxn3b +/+ littermates. This aberrant immune compartmentalization is recapitulated in uninfected Ubxn3b -/- mice. Mechanistically, UBXN3B controls precursor B-I (pre-BI) transition to pre-BII and subsequent proliferation in a cell-intrinsic manner, by maintaining BLNK protein stability and pre-BCR signaling. These results reveal an essential role of UBXN3B for the early stage of B cell development.

    Citation

    Tingting Geng, Duomeng Yang, Tao Lin, Andrew G Harrison, Binsheng Wang, Blake Torrance, Kepeng Wang, Yanlin Wang, Long Yang, Laura Haynes, Gong Cheng, Anthony T Vella, Erol Fikrig, Penghua Wang. An Essential Role of UBXN3B in B Lymphopoiesis. bioRxiv : the preprint server for biology. 2021 Aug 24


    PMID: 34462748

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