Abstract:
:The terminal differentiation of B cells into antibody-secreting cells (ASCs) is a critical component of adaptive immune responses. However, it is a very sensitive process, which dysfunctions lead to a great variety of lymphoproliferative neoplasia including germinal center-derived lymphomas. To better characterize the late genomic events driving the ASC differentiation of human primary naive B cells, we used our in vitro differentiation system and a combination of RNA sequencing with ATAC-seq. Our results evidenced two mechanisms driving human terminal B cell differentiation. Firstly, after an initial response to IL-4, cells that committed to an ASC fate downregulated the CD23 marker and IL-4 signaling, whereas cells that maintained IL-4 signaling did not differentiate. Secondly, human CD23-negative cells also increased IRF4 protein to levels required for ASC differentiation, but independently of the ubiquitin-mediated degradation process previously described in the mouse. Finally, we showed that CD23-negative cells (i) carried the imprint of their previous activated B-cell status, (ii) were precursors of plasmablasts, and (iii) had a similar phenotype to in vivo pre-plasmablasts. Altogether, our results provide an unprecedented genomic characterization of the fate decision between activated B cells and plasmablast, which gives new insights in pathological mechanisms driving lymphoma biology.
journal_name
Bloodjournal_title
Bloodauthors
Pignarre A,Chatonnet F,Caron G,Haas M,Desmots-Loyer F,Fest Tdoi
10.1182/blood.2020005083subject
Has Abstractpub_date
2020-11-04 00:00:00eissn
0006-4971issn
1528-0020pii
474072pub_type
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