| First Author | Azar AA | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 13156 |
| PubMed ID | 32753714 | Mgi Jnum | J:298814 |
| Mgi Id | MGI:6457738 | Doi | 10.1038/s41598-020-70191-y |
| Citation | Azar AA, et al. (2020) A novel transgenic mouse strain expressing PKCbetaII demonstrates expansion of B1 and marginal zone B cell populations. Sci Rep 10(1):13156 |
| abstractText | Protein kinase Cbeta (PKCbeta) expressed in mammalian cells as two splice variants, PKCbetaI and PKCbetaII, functions in the B cell receptor (BCR) signaling pathway and contributes to B cell development. We investigated the relative role of PKCbetaII in B cells by generating transgenic mice where expression of the transgene is directed to these cells using the Emicro promoter (Emicro-PKCbetaIItg). Our findings demonstrate that homozygous Emicro-PKCbetaIItg mice displayed a shift from IgD(+)IgM(dim) toward IgD(dim)IgM(+) B cell populations in spleen, peritoneum and peripheral blood. Closer examination of these tissues revealed respective expansion of marginal zone (MZ)-like B cells (IgD(+)IgM(+)CD43(neg)CD21(+)CD24(+)), increased populations of B-1 cells (B220(+)IgD(dim)IgM(+)CD43(+)CD24(+)CD5(+)), and higher numbers of immature B cells (IgD(dim)IgM(dim)CD21(neg)) at the expense of mature B cells (IgD(+)IgM(+)CD21(+)). Therefore, the overexpression of PKCbetaII, which is a phenotypic feature of chronic lymphocytic leukaemia cells, can skew B cell development in mice, most likely as a result of a regulatory influence on BCR signaling. |
