| First Author | Adori M | Year | 2023 |
| Journal | Cells | Volume | 12 |
| Issue | 9 | PubMed ID | 37174629 |
| Mgi Jnum | J:359337 | Mgi Id | MGI:7483158 |
| Doi | 10.3390/cells12091229 | Citation | Adori M, et al. (2023) Enhanced B Cell Receptor Signaling Partially Compensates for Impaired Toll-like Receptor 4 Responses in LPS-Stimulated IkappaBNS-Deficient B Cells. Cells 12(9) |
| abstractText | Lipopolysaccharide (LPS) stimulates dual receptor signaling by bridging the B cell receptor and Toll-like receptor 4 (BCR/TLR4). B cells from IkappaBNS-deficient bumble mice treated with LPS display reduced proliferative capacity and impaired plasma cell differentiation. To improve our understanding of the regulatory role of IkappaBNS in B cell activation and differentiation, we investigated the BCR and TLR4 signaling pathways separately by using dimeric anti-IgM Fab (F(ab')(2)) or lipid A, respectively. IkappaBNS-deficient B cells exhibited reduced survival and defective proliferative capacity in response to lipid A compared to B cells from wildtype (wt) control mice. In contrast, anti-IgM stimulation of bumble B cells resulted in enhanced viability and increased differentiation into CD138(+) cells compared to control B cells. Anti-IgM-stimulated IkappaBNS-deficient B cells also showed enhanced cycle progression with increased levels of c-Myc and cyclin D2, and augmented levels of pCD79a, pSyk, and pERK compared to control B cells. These results suggest that IkappaBNS acts as a negative regulator of BCR signaling and a positive regulator of TLR4 signaling in mouse B cells. |
