It has been almost 50 years since autoantibodies (Abs) were identified in the blood of patients with myositis.1 Since then, the targets of several myositis-specific antibodies (MSAs) have been identified as ubiquitous proteins involved in critical cellular processes, such as protein translation, DNA repair, transcription, and viral recognition.2 Several pieces of evidence suggest that these Abs are not merely epiphenomena but are markers of an immune response that is central to disease propagation: the most compelling of these is the finding that patients typically have only 1 MSA type (eg, Mi-2 vs Jo-1), and those with a particular MSA often share similar clinical features regarding organ system involvement, prognosis, and response to therapy.3,4
Fiorentino D, Werth VP. Dermatomyositis Autoantibodies: Clinical Markers of Patients Past, Present, and Future. Arch Dermatol. 2011;147(4):492–494. doi:10.1001/archdermatol.2011.41
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