Presenting Author: Penghua Wang
, Associate Professor at UConn Hlth.
Abstract:
Hematopoiesis is finely regulated to enable timely production of the right numbers and types of immune cells. Herein, we report the crucial function of UBXN3B in B lymphopoiesis. In an inducible global knockout mouse model, we observe a striking reduction in B, a moderate decrease in T, while increase in myeloid populations. The B lineage deficiency begins from the small precursor B and is recapitulated in B cell-specific Ubxn3bknockout. Transfer of wildtype bone marrows to irradiated global Ubxn3bknockout restores the B population, while reverse transplantation fails. Following induction of Ubxn3b knockout, the peripheral B population drops rapidly with significant apoptosis. Ubxn3b deficiency renders mice highly vulnerable to respiratory viruses, typified by reduced B population and virus-specific antibodies, increased myeloid populations and lung immunopathology. This study reveals a cell-intrinsic essential role of UBXN3B in B cell survival and UBXN3B as a potential therapeutic target for B-cell related diseases.
The Essential Role of UBXN3B in B Lymphopoiesis and Survival
Category
Poster and Podium (Block Symposium)
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Date: May 5 Presentation Time: 11:30 AM to 12:45 PM Room: Exhibit Hall F1