| First Author | Tian M | Year | 2018 |
| Journal | J Immunol | Volume | 200 |
| Issue | 3 | Pages | 937-948 |
| PubMed ID | 29282308 | Mgi Jnum | J:258131 |
| Mgi Id | MGI:6112963 | Doi | 10.4049/jimmunol.1701067 |
| Citation | Tian M, et al. (2018) B Cell-Intrinsic MyD88 Signaling Promotes Initial Cell Proliferation and Differentiation To Enhance the Germinal Center Response to a Virus-like Particle. J Immunol 200(3):937-948 |
| abstractText | Although TLR signaling in B cells has been implicated in the germinal center (GC) responses during viral infections and autoimmune diseases, the underlying mechanism is unclear. Bacterial phage Qbeta-derived virus-like particle (Qbeta-VLP) contains TLR ligands, which can enhance Qbeta-VLP-induced Ab response, including GC response, through TLR/MyD88 signaling in B cells. In this study, by examining Ag-specific B cell response to Qbeta-VLP, we found that lack of B cell MyD88 from the beginning of the immune response led to a more severe defect in the GC scale than abolishing MyD88 at later time points of the immune response. Consistently, B cell-intrinsic MyD88 signaling significantly enhanced the initial proliferation of Ag-specific B cells, which was accompanied with a dramatic increase of plasma cell generation and induction of Bcl-6(+) GC B cell precursors. In addition, B cell-intrinsic MyD88 signaling promoted strong T-bet expression independent of IFN-gamma and led to the preferential isotype switching to IgG2a/c. Thus, by promoting the initial Ag-specific B cell proliferation and differentiation, B cell-intrinsic MyD88 signaling enhanced both T-independent and T-dependent Ab responses elicited by Qbeta-VLP. This finding will provide additional insight into the role of TLR signaling in antiviral immunity, autoimmune diseases, and vaccine design. |
