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One of eight autoantibodies against the aminoacyl-transferase RNA synthetases (ARS) is detectable in the serum of affected patients. However, disease-specific therapeutic approaches have not yet been established.<\/jats:p>\n                  <jats:p>\n                    To obtain a deeper understanding of the underlying pathogenesis and to identify putative therapeutic targets, we comparatively investigated the most common forms of ASyS associated with anti-PL-7, anti-PL-12 and anti-Jo-1. Our cohort consisted of 80 ASyS patients as well as healthy controls (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200940), diseased controls (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200940) and non-diseased controls (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200920). We detected a reduced extent of necrosis and regeneration in muscle biopsies from PL-12\n                    <jats:sup>+<\/jats:sup>\n                    patients compared to Jo-1\n                    <jats:sup>+<\/jats:sup>\n                    patients, while PL-7\n                    <jats:sup>+<\/jats:sup>\n                    patients had higher capillary dropout in biopsies of skeletal muscle. Aside from these subtle alterations, no significant differences between ASyS subgroups were observed. Interestingly, a tissue-specific subpopulation of CD138\n                    <jats:sup>+<\/jats:sup>\n                    plasma cells and CXCL12\n                    <jats:sup>+<\/jats:sup>\n                    \/CXCL13\n                    <jats:sup>+<\/jats:sup>\n                    CD20\n                    <jats:sup>+<\/jats:sup>\n                    B cells common to ASyS myositis were identified. These cells were localized in the endomysium associated with alkaline phosphatase\n                    <jats:sup>+<\/jats:sup>\n                    activated mesenchymal fibroblasts and CD68\n                    <jats:sup>+<\/jats:sup>\n                    MHC-II\n                    <jats:sup>+<\/jats:sup>\n                    CD169\n                    <jats:sup>+<\/jats:sup>\n                    macrophages. An MHC-I\n                    <jats:sup>+<\/jats:sup>\n                    and MHC-II\n                    <jats:sup>+<\/jats:sup>\n                    MxA negative type II interferon-driven milieu of myofiber activation, topographically restricted to the perifascicular area and the adjacent perimysium, as well as perimysial clusters of T follicular helper cells defined an extra-medullary immunological niche for plasma cells and activated B cells. Consistent with this, proteomic analyses of muscle tissues from ASyS patients demonstrated alterations in antigen processing and presentation. In-depth immunological analyses of peripheral blood supported a B-cell\/plasma-cell-driven pathology with a shift towards immature B cells, an increase of B-cell-related cytokines and chemokines, and activation of the complement system. We hypothesize that a B-cell-driven pathology with the presence and persistence of a specific subtype of plasma cells in the skeletal muscle is crucially involved in the self-perpetuating chronicity of ASyS myositis. This work provides the conceptual framework for the application of plasma-cell-targeting therapies in ASyS myositis.\n                  <\/jats:p>","DOI":"10.1007\/s00401-022-02438-z","type":"journal-article","created":{"date-parts":[[2022,5,25]],"date-time":"2022-05-25T05:04:37Z","timestamp":1653455077000},"page":"353-372","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":58,"title":["Skeletal muscle provides the immunological micro-milieu for specific plasma cells in anti-synthetase syndrome-associated 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