MyD88 Is Required for the Formation of Long-Term Humoral Immunity to Virus Infection

摘要: Development of long-term humoral immunity is a major goal vaccination, but the mechanisms involved in formation Ab responses are still being determined. In this study, we identify previously unknown requirement for MyD88, an adaptor molecule that mediates signals at most TLRs, generation during live virus infection. Polyoma virus-infected MyD88 knockout mice generated strong acute T cell-dependent antiviral IgM and IgG developed germinal centers. Activation-induced cytidine deaminase, enzyme required isotype switching somatic hypermutation, was also induced center B cells, similar to wild-type mice. However, failed develop bone marrow plasma cells did not maintain serum responses. The distribution altered; IgG2a IgG2b levels were diminished, whereas IgG1 affected. polyoma intrinsic independent IL-1R IL-18R, cytokine receptors signal through MyD88. Our findings show MyD88-dependent signaling pathways essential effectively generating implicate role TLR immunity.