TLR7 and myositis disease: First, laboratory-based studies in our unique model of HRS-induced myositis do not completely explain the mechanistic basis for these overlapping immune responses or fully define the role of Type I IFN signaling in promoting anti-Ro52 and/or anti-Ro60 immunity (given the relatively robust anti-Ro52 and anti-Ro60 immune responses to HRS immunization in the absence of IFA and the TLR7/8 agonist, R848; Supplementary Figure 3).