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The major clinical and autoantibody phenotypes in children have many features similar to those in adults, and each has distinct demographic and clinical features and associated outcomes. The most common myositis autoantibodies in\n                    <jats:styled-content style=\"fixed-case\">JIIM<\/jats:styled-content>\n                    patients are anti\u2010p155\/140, anti\u2010\n                    <jats:styled-content style=\"fixed-case\">MJ<\/jats:styled-content>\n                    and anti\u2010\n                    <jats:styled-content style=\"fixed-case\">MDA<\/jats:styled-content>\n                    5. Higher mortality has been associated with overlap myositis as well as with the presence of anti\u2010synthetase and anti\u2010\n                    <jats:styled-content style=\"fixed-case\">MDA<\/jats:styled-content>\n                    5 autoantibodies; a chronic illness course and lipodystrophy have been associated with anti\u2010p155\/140 autoantibodies; and calcinosis has been associated with anti\u2010\n                    <jats:styled-content style=\"fixed-case\">MJ<\/jats:styled-content>\n                    autoantibodies. Histologic abnormalities of\n                    <jats:styled-content style=\"fixed-case\">JIIM<\/jats:styled-content>\n                    s detectable on muscle biopsy have also been correlated with myositis\u2010specific autoantibodies; for example, patients with anti\u2010\n                    <jats:styled-content style=\"fixed-case\">MDA<\/jats:styled-content>\n                    5 show low levels of inflammatory infiltrate and muscle damage on biopsy. The first genome\u2010wide association study of adult and juvenile dermatomyositis revealed three novel genetic associations,\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">BLK<\/jats:styled-content>\n                    <\/jats:italic>\n                    ,\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">PLCL<\/jats:styled-content>\n                      1\n                    <\/jats:italic>\n                    and\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>\n                      21\n                    <\/jats:italic>\n                    and confirmed that the human leucocyte antigen region is the primary risk region for juvenile dermatomyositis. Here, we review the well\u2010established pathogenic processes in\n                    <jats:styled-content style=\"fixed-case\">JIIM<\/jats:styled-content>\n                    s, including the type 1 interferon and endoplasmic reticulum stress pathways. Several novel\n                    <jats:styled-content style=\"fixed-case\">JIIM<\/jats:styled-content>\n                    \u2010associated inflammatory mediators, such as the innate immune system proteins, myeloid\u2010related peptide 8\/14, galectin 9 and eotaxin, have emerged as promising biomarkers of disease. Advances in our understanding of the phenotypes and pathophysiology of the\n                    <jats:styled-content style=\"fixed-case\">JIIM<\/jats:styled-content>\n                    s are leading to better tools to help clinicians stratify and treat these heterogeneous disorders.\n                  <\/jats:p>","DOI":"10.1111\/joim.12444","type":"journal-article","created":{"date-parts":[[2016,3,31]],"date-time":"2016-03-31T23:19:03Z","timestamp":1459466343000},"page":"24-38","source":"Crossref","is-referenced-by-count":150,"title":["The juvenile idiopathic inflammatory myopathies: pathogenesis, clinical and autoantibody phenotypes, and outcomes"],"prefix":"10.1111","volume":"280","author":[{"given":"L. 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