RESULTS: IBM exhibited a homogeneous and distinct proteomic signature compared with other IIM subtypes, driven by upregulation of MHC class I (e.g. HLA-A) and II (e.g. HLA-DRB1, CD74) molecules, and cytoskeletal proteins (e.g. PDCL3). This evidence concerns the gene HLA-DRB1 and inclusion body myositis.