Abstract
AbstractOver the recent decades, notable progress has been made in the understanding of the pathomechanism of autoimmune myositis. Dermatomyositis is considered a type I interferonopathy, distinctive from antisynthetase syndrome despite some common clinical features. Immune‐mediated necrotizing myopathy is related to complement‐mediated autoimmunity. In inclusion body myositis, myofiber invasion by highly differentiated cytotoxic T cells leads to myofiber damage. Based on the accumulated knowledge, targeted, more mechanism‐focused therapies are being developed.
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