| First Author | Rubtsov AV | Year | 2008 |
| Journal | J Immunol | Volume | 180 |
| Issue | 6 | Pages | 3882-8 |
| PubMed ID | 18322196 | Mgi Jnum | J:132917 |
| Mgi Id | MGI:3777194 | Doi | 10.4049/jimmunol.180.6.3882 |
| Citation | Rubtsov AV, et al. (2008) TLR Agonists Promote Marginal Zone B Cell Activation and Facilitate T-Dependent IgM Responses. J Immunol 180(6):3882-8 |
| abstractText | Although IgM serves as a first barrier to Ag spreading, the cellular and molecular mechanisms following B lymphocyte activation that lead to IgM secretion are not fully understood. By virtue of their anatomical location, marginal zone (MZ) B cells rapidly generate Ag-specific IgM in response to blood-borne pathogens and play an important role in the protection against these potentially harmful Ags. In this study, we have explored the contribution of TLR agonists to MZ B cell activation and mobilization as well as their ability to promote primary IgM responses in a mouse model. We demonstrate that diverse TLR agonists stimulate MZ B cells to become activated and leave the MZ through pathways that are differentially dependent on MyD88 and IFN-alphabeta receptor signaling. Furthermore, in vivo stimulation of MZ B cells with TLR agonists led to a reduction in the expression of the sphingosine-1-phosphate (S1P) receptors expressed by MZ B cells and/or increased CD69 cell surface levels. Importantly, as adjuvants for a T cell-dependent protein Ag, TLR agonists were found to accelerate the kinetics but not magnitude of the Ag-specific IgM response. Together, these data demonstrate that in vivo TLR agonist treatment enhances the early production of Ag-specific IgM and activates MZ B cells to promote their relocation. |
