| First Author | Meyer-Bahlburg A | Year | 2007 |
| Journal | J Exp Med | Volume | 204 |
| Issue | 13 | Pages | 3095-101 |
| PubMed ID | 18039950 | Mgi Jnum | J:130405 |
| Mgi Id | MGI:3771644 | Doi | 10.1084/jem.20071250 |
| Citation | Meyer-Bahlburg A, et al. (2007) B cell intrinsic TLR signals amplify but are not required for humoral immunity. J Exp Med 204(13):3095-101 |
| abstractText | Although innate signals driven by Toll-like receptors (TLRs) play a crucial role in T-dependent immune responses and serological memory, the precise cellular and time-dependent requirements for such signals remain poorly defined. To directly address the role for B cell-intrinsic TLR signals in these events, we compared the TLR response profile of germinal center (GC) versus naive mature B cell subsets. TLR responsiveness was markedly up-regulated during the GC reaction, and this change correlated with altered expression of the key adaptors MyD88, Mal, and IRAK-M. To assess the role for B cell-intrinsic signals in vivo, we transferred MyD88 wild-type or knockout B cells into B cell-deficient microMT mice and immunized recipient animals with 4-hydroxy-3-nitrophenylacetyl (NP) chicken gamma globulin. All recipients exhibited similar increases in NP-specific antibody titers during primary, secondary, and long-term memory responses. The addition of lipopolysaccharide to the immunogen enhanced B cell-intrinsic, MyD88-dependent NP-specific immunoglobulin (Ig)M production, whereas NP-specific IgG increased independently of TLR signaling in B cells. Our data demonstrate that B cell-intrinsic TLR responses are up-regulated during the GC reaction, and that this change significantly promotes antigen-specific IgM production in association with TLR ligands. However, B cell-intrinsic TLR signals are not required for antibody production or maintenance. |
