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Publication : CCAAT/enhancer binding protein β Induces Post-Switched B Cells to Produce Blimp1 and Differentiate into Plasma Cells.

First Author  Lee G Year  2020
Journal  Immune Netw Volume  20
Issue  5 Pages  e42
PubMed ID  33163250 Mgi Jnum  J:352843
Mgi Id  MGI:7704317 Doi  10.4110/in.2020.20.e42
Citation  Lee G, et al. (2020) CCAAT/enhancer binding protein beta Induces Post-Switched B Cells to Produce Blimp1 and Differentiate into Plasma Cells. Immune Netw 20(5):e42
abstractText  Long-lasting post-switched plasma cells (PCs) arise mainly from germinal center (GC) reactions, but little is known about the mechanism by which GC B cells differentiate into PCs. Based on our observation that the expression of the transcription factor CCAAT/enhancer binding protein beta (C/EPBbeta) is associated with the emergence of post-switched PCs, we enquired whether a cell-autonomous function of C/EPBbeta is involved in the program for PC development. To address this, we generated C/EPBbeta-deficient mice in which the Cebpb locus was specifically deleted in B cells after transcription of the Ig gamma1 constant gene segment (Cgamma1). In response to in vitro stimulation, B cells from these Cebpb(fl/fl)Cgamma1(Cre/+) mice had defects in the induction of B lymphocyte-induced maturation protein 1 (Blimp1) and the formation of IgG1(+) PCs, but not in proliferation and survival. At steady state, the Cebpb(fl/fl)Cgamma1(Cre/+) mice had reduced serum IgG1 titers but normal IgG2c and IgM titers. Moreover, upon immunization with T-dependent Ag, the mice produced reduced levels of Ag-specific IgG1 Ab, and were defective in the production of Ag-specific IgG1 Ab-secreting cells. These results suggest that a cell-autonomous function of C/EPBbeta is crucial for differentiation of post-switched GC B cells into PCs through a Blimp1-dependent pathway.
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