Myositis autoantibodies: from new specificities to new paradigms

Myositis-specific autoantibodies have long been used to classify patients into clinically meaningful subsets; however, recent studies show that the field is moving beyond the simple question of which autoantibody is present. This review examines how emerging specificities, epitope architecture, autoantibody coexistence, pathogenic mechanisms, and detection platforms are reshaping the interpretation of myositis serology.

Recent work has expanded the autoantibody repertoire through the identification of additional autoantibody specificities, multiprotein antigenic complexes, and transcriptional regulators. At the same time, epitope-level studies reveal that patients sharing the same autoantibody specificity may recognize different antigenic regions, with potential implications for phenotype, prognosis, and assay interpretation. Evidence also challenges the view of myositis autoantibodies as passive biomarkers: selected specificities may mediate complement-dependent muscle injury, amplify inflammatory circuits, or interfere with intracellular antigen function. Meanwhile, new detection platforms have not only improved discovery but also exposed limitations related to conformational epitopes, cross-reactivity, false seronegativity, and assay standardization.

Novelty in myositis autoantibodies should be understood not only as new targets but also as new paradigms linking antigen structure, immune mechanisms, detection methods, and clinical actionability.