{"id":72312,"date":"2026-08-06T00:08:38","date_gmt":"2026-08-05T22:08:38","guid":{"rendered":"https:\/\/inmuno.es\/index.php\/2026\/08\/06\/il-17-driven-transcriptional-programs-in-muscle-fibroblasts-are-not-required-for-pathogenesis-in-murine-anti-histidyl-trna-synthetase-jo-1-myositis\/"},"modified":"2026-08-06T00:08:38","modified_gmt":"2026-08-05T22:08:38","slug":"il-17-driven-transcriptional-programs-in-muscle-fibroblasts-are-not-required-for-pathogenesis-in-murine-anti-histidyl-trna-synthetase-jo-1-myositis","status":"publish","type":"post","link":"https:\/\/inmuno.es\/index.php\/2026\/08\/06\/il-17-driven-transcriptional-programs-in-muscle-fibroblasts-are-not-required-for-pathogenesis-in-murine-anti-histidyl-trna-synthetase-jo-1-myositis\/","title":{"rendered":"IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis"},"content":{"rendered":"<div>\n<p><b>J Immunol<\/b>. 2026 Aug 4;215(8):vkag225. doi: 10.1093\/jimmun\/vkag225.<\/p>\n<p><b>ABSTRACT<\/b><\/p>\n<p>Idiopathic inflammatory myopathy (IIM) is a systemic autoimmune disease targeting muscle and extramuscular organs, but the molecular mechanisms driving IIM pathogenesis remain largely undefined. Muscle fibroblasts are central to orchestrating inflammation in myositis. Here, we investigated muscle fibroblast dynamics using a single-cell RNA sequencing approach in an established murine model of anti-histidyl-tRNA synthetase (HRS, also known as Jo-1)-induced myositis. In fibroblasts, there was a robust activation of an IL-17 gene signature during disease. Among the induced genes was Nfkbiz, which encodes I\u03baB\u03b6, a noncanonical NF-\u03baB transcriptional coactivator known to be key for pathologic IL-17 signaling in a variety of autoimmune settings. In muscle fibroblasts, I\u03baB\u03b6 was potently activated by IL-17 in vitro and was essential for IL-17 signaling responsiveness. Surprisingly, however, the IL-17-I\u03baB\u03b6 signaling axis was dispensable for the histopathological phenotype in HRS-induced myositis. Thus, despite a prominent IL-17 transcriptional signature, IL-17 and I\u03baB\u03b6 are not required for autoantibody production or tissue inflammation in this model system.<\/p>\n<p>PMID:<a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/42554729\/?utm_source=SimplePie&amp;utm_medium=rss&amp;utm_content=2985117R&amp;ff=20260805180837&amp;v=2.20.1\">42554729<\/a> | DOI:<a href=\"https:\/\/doi.org\/10.1093\/jimmun\/vkag225\">10.1093\/jimmun\/vkag225<\/a><\/p>\n<\/div>","protected":false},"excerpt":{"rendered":"<p>J Immunol. 2026 Aug 4;215(8):vkag225. doi: 10.1093\/jimmun\/vkag225. ABSTRACT Idiopathic inflammatory myopathy (IIM) is a systemic autoimmune disease targeting muscle and extramuscular organs, but the molecular mechanisms driving IIM pathogenesis remain largely undefined. Muscle fibroblasts are central to orchestrating inflammation in myositis. Here, we investigated muscle fibroblast dynamics using a single-cell RNA sequencing approach in an &#8230; <a title=\"IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis\" class=\"read-more\" href=\"https:\/\/inmuno.es\/index.php\/2026\/08\/06\/il-17-driven-transcriptional-programs-in-muscle-fibroblasts-are-not-required-for-pathogenesis-in-murine-anti-histidyl-trna-synthetase-jo-1-myositis\/\" aria-label=\"Read more about IL-17-driven transcriptional programs in muscle fibroblasts are not required for pathogenesis in murine anti-histidyl-tRNA synthetase (Jo-1) myositis\">Read more<\/a><\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[42,71],"tags":[],"class_list":["post-72312","post","type-post","status-publish","format-standard","hentry","category-publicaciones","category-the-journal-of-immunology"],"_links":{"self":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts\/72312","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/comments?post=72312"}],"version-history":[{"count":0,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/posts\/72312\/revisions"}],"wp:attachment":[{"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/media?parent=72312"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/categories?post=72312"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/inmuno.es\/index.php\/wp-json\/wp\/v2\/tags?post=72312"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}