Although deletion of MyD88 signaling in B cells is sufficient to abrogate lupus nephritis in the MRL/lpr and Lyn−/− mouse models 26,39, MyD88 deficiency in dendritic cells (DCs) can also confer some protection and highlights the cooperation between B cells and DCs 26,63, and potentially other (nonhematopoietic) cells, in the development of SLE-like pathologies. Here, MYD88 is linked to systemic lupus erythematosus.