Polymyositis (PM) and dermatomyositis (DM) represent a group of chronic inflammatory disorders characterized by myogenic changes, skin eruptions, or both. Clinical features are heterogeneous, with various degrees of skin manifestations, myositis, and pulmonary involvement, which considerably determine the severity and prognosis.
1 Although the causes of these disorders remain unclear, autoimmunity is considered to have a critical role because the presence of diagnostic autoantibodies (Abs), known as myositis-related Abs, is a prominent feature.
2 A variety of serum Abs are detected in patients with PM/DM, including Abs reactive with aminoacyltransfer RNA synthetase (ARS),
3 signal recognition particle,
4 and Mi-2.
5 These Abs are associated with clinically distinct subsets of PM/DM, that is, anti-ARS with interstitial lung disease (ILD), arthritis, Raynaud phenomenon, and mechanic hand
6,7; anti–signal recognition particle with acute-onset severe refractory PM
8-10; and anti–Mi-2 with typical DM with a lower risk of ILD and internal malignancy and good response to treatment.
11-13 In addition, anti–PM-Scl, anti-Ku, and anti-U1RNP Abs are associated with myositis overlap syndrome.
14 Therefore, identification of myositis-related Abs is useful in defining clinically homogenous patient subsets, in predicting prognosis, and in clarifying the pathogenesis. Recently, 2 myositis-related Abs, anti–155/140
15,16 and anti–CADM-140,
17 have been reported. Subsequent studies have revealed corresponding autoantigens: transcriptional intermediary factor 1-γ for anti–155/140
18 and melanoma differentiation–associated gene 5 for anti–CADM-140.
19 Anti–155/140 Abs are reported to represent malignancy-associated or juvenile DM,
15,20 and anti–CADM-140 Abs are reported to be associated with amyopathic DM and rapidly progressive ILD (RP-ILD).
17,19 Although precise clinical details of these 2 Abs need to be clarified further, anti–155/140, anti–CADM-140, and anti–Mi-2 Abs are considered to be highly specific for DM.