| First Author | Guay HM | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 8 | Pages | 5124-31 |
| PubMed ID | 17404295 | Mgi Jnum | J:145278 |
| Mgi Id | MGI:3834065 | Doi | 10.4049/jimmunol.178.8.5124 |
| Citation | Guay HM, et al. (2007) MyD88 is required for the formation of long-term humoral immunity to virus infection. J Immunol 178(8):5124-31 |
| abstractText | Development of long-term humoral immunity is a major goal of vaccination, but the mechanisms involved in the formation of long-term Ab responses are still being determined. In this study, we identify a previously unknown requirement for MyD88, an adaptor molecule that mediates signals at most TLRs, for the generation of long-term humoral immunity during live virus infection. Polyoma virus-infected MyD88 knockout mice generated strong acute T cell-dependent antiviral IgM and IgG responses and developed germinal centers. Activation-induced cytidine deaminase, an enzyme required for isotype switching and somatic hypermutation, was also induced in germinal center B cells, similar to wild-type mice. However, MyD88 knockout mice failed to develop bone marrow plasma cells and did not maintain long-term serum antiviral Ab responses. The isotype distribution of antiviral IgG responses was also altered; serum IgG2a and IgG2b levels were diminished, whereas IgG1 responses were not affected. The requirement for MyD88 for the formation of long-term humoral immunity to polyoma virus was intrinsic to B cells and was independent of IL-1R and IL-18R, cytokine receptors that also signal through MyD88. Our findings show that MyD88-dependent signaling pathways in B cells are essential for effectively generating long-term Ab responses and implicate a role for TLR in the formation of long-term humoral immunity. |
