Abstract
Autoantibodies targeting intracellular proteins involved in key processes are detected in patients with idiopathic inflammatory myopathies. These myositisspecific autoantibodies have been increasingly demonstrated to correlate with distinct clinical phenotypes within the myositis spectrum. This review highlights the clinical associations of the myositisspecific autoantibodies, with particular attention to the recently identified and characterized novel myositis autoantibodies: p155/140, p140 (MJ), CADM-140 (MDA5), SAE, and 200/100.
Highlights
The idiopathic inflammatory myopathies (IIMs) polymyositis (PM) and dermatomyositis (DM) are heterogeneous conditions that are historically diagnosed by proximal muscle weakness, evidence of muscle inflammation or necrosis, and characteristic skin lesions [1,2]
It is well recognized that patients can present with other overlapping features, including arthritis and systemic involvement, and this has led to the proposal of alternative diagnostic criteria [3]
The increasing number of patients with a known myositis-specific autoantibody (MSA) aids the clinicoserological classification of myositis and may help to predict complications of disease, prognosis, and responses to treatment
Summary
The idiopathic inflammatory myopathies (IIMs) polymyositis (PM) and dermatomyositis (DM) are heterogeneous conditions that are historically diagnosed by proximal muscle weakness, evidence of muscle inflammation or necrosis, and characteristic skin lesions [1,2]. IIM and are directed to specific proteins found in both the nuclear and cytoplasmic regions of the cell; these MSAs correlate with genotype and clinical manifestations [4,5]. Investigations into these specific autoantibodies help classify myositis patients into increasingly homogeneous subgroups, may guide specific treatment regimes, and importantly increase our understanding of the pathogenesis of IIM. The ‘traditional’ MSAs – anti-Jo-1 (and the less common non-Jo-1 anti-synthetases), anti-SRP, and antiMi-2 – can be detected by routine commercial assays and are identified in approximately 40% to 50% of adult myositis patients and in less than 10% of juvenile dermatomyositis (JDM) patients [6].
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