Both IFNα2 and IFNβ1 have been reported to induce or exacerbate dermatomyositis and polymyositis in some patients [82,83], and it have been suggested that as in the case of SLE and SS, RNA or DNA contained in soluble immune complexes taken up by pDCs interacts with TLRs in endosomal vesicles leading to local over-production of type I IFNs in skin and muscle [80,81,82]. This evidence concerns the gene IFNA2 and synovial sarcoma.