ABSTRACT
Considerable in vitro data over the past decade have pointed to a critical role for TLR9 and TLR7 in the activation of autoantibody-producing B cells and IFN-αproducing plasmacytoid dendritic cells. However, it is only within the past year that the availability of the appropriate TLR-targeted autoimmune-prone strains has made it possible to formally test the Toll hypothesis in vivo. As anticipated, these studies have indicated that both TLR9 and TLR7 play an important role in the activation of autoreactive B cells. However, unexpectedly, TLR9 deficiency appeared to exacerbate rather than improve the overall level of clinical disease. Potential mechanisms and implications for further studies will be discussed in this review.
