Myositis-specific autoantibodies are often associated with particular clinical features. Myositis-specific autoantibodies, present in 60–70% of individuals with IIM, are directed against cytoplasmic or nuclear components involved in key intracellular processes, including protein synthesis and chromatin re-modelling 2. Viral and bacterial infections have been reported in IIM 1, but their role in disease pathology is unclear.Īutoantibodies are a key feature of IIM, in common with other autoimmune rheumatic diseases such as rheumatoid arthritis, systemic lupus erythematosus and systemic sclerosis. IIM are thought to result from immune activation following environmental exposures in genetically susceptible individuals. The idiopathic inflammatory myopathies (IIM) are a heterogeneous spectrum of rare autoimmune musculoskeletal diseases characterised clinically by muscle weakness and systemic organ involvement. Our findings indicate that molecular mimicry and epitope spreading events may play a role in dermatomyositis pathogenesis. Our data suggest antibody accumulation in dermatomyositis against an expanded diversity of microbial and human proteins and evidence of non-random targeting of specific signalling pathways. Some of these TRIM proteins share epitope homology with specific viral species including poxviruses. In addition to TRIM33, we identify autoantibodies against eleven further TRIM proteins, including TRIM21. The identified autoantibodies recognise a large portion of the human proteome, including interferon regulated proteins these proteins cluster in specific biological processes. Antibodies recognizing viruses and Poxviridae family species are significantly enriched. We observe antibodies recognizing a wider repertoire of microbial antigens in dermatomyositis. We use an untargeted high-throughput approach which combines immunoglobulin disease-specific epitope-enrichment and identification of microbial and human antigens. We investigate the accumulated microbial and autoantigen antibody repertoire in adult-onset dermatomyositis patients sero-positive for TIF1γ (TRIM33) autoantibodies.
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