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Idiopathic inflammatory myopathies (IIMs) are rare, heterogeneous, autoimmune musculoskeletal diseases, characterised clinically by muscle weakness. Extramuscular involvement includes the skin, respiratory and cardiovascular systems. Genetic and environmental factors contribute to IIM susceptibility, and viral or bacterial infection may contribute to disease pathogenesis.
Both the innate and adaptive immune systems are important in IIM pathology. Two-thirds of affected individuals have known myositis-specific or associated autoantibodies, often linked to particular clinical features,1 and directed against proteins involved in key intracellular processes. Interferon pathways are differentially activated in clinical subtypes of myositis2; this interferon response is critical to protect the host against viral infection and modulate the antiviral immune response.
We recently used a high-throughput approach combining disease-specific immunoglobulin epitope signature enrichment and antigen identification from the total microbial ‘exposome’ (including viruses, bacteria, archaea and fungi) and human proteins.3 We applied this serum antibody repertoire analysis pipeline to investigate the microbial and autoantigen antibody repertoire accumulated throughout life in 20 adult-onset dermatomyositis patients seropositive for TIF1γ (TRIM33) autoantibodies, compared with 20 age-matched and gender-matched healthy controls.3
Human coronaviruses are associated with the common cold, but can lead to fatal inflammatory responses and acute lung injury. Emergence of a novel coronavirus …
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