{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,8]],"date-time":"2026-08-08T22:59:49Z","timestamp":1786229989002,"version":"build-2736575974"},"reference-count":20,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,2,23]],"date-time":"2026-02-23T00:00:00Z","timestamp":1771804800000},"content-version":"vor","delay-in-days":22,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"},{"start":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T00:00:00Z","timestamp":1769904000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004628","name":"MedImmune","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004628","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000066","name":"National Institute of Environmental Health Sciences","doi-asserted-by":"publisher","award":["NIEHS; ZIAES101074"],"award-info":[{"award-number":["NIEHS; ZIAES101074"]}],"id":[{"id":"10.13039\/100000066","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","award":["NIAMS; ZIDAR041180"],"award-info":[{"award-number":["NIAMS; ZIDAR041180"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["acrjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["ACR Open Rheumatology"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Transcript and protein abundance data were measured to compare biologic pathway effects in the peripheral blood of patients diagnosed with systemic lupus erythematosus (SLE) and dermatomyositis (DM) who receive immunosuppressive therapies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Expression data from the peripheral blood of patients with SLE (n = 41) and DM (n = 14) were obtained using one transcriptomic and two proteomic platforms and compared with matched healthy control subjects. Regulatory effects were integrated across the three platforms to assess biologic pathways and downstream signaling, within and across disease cohorts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Expressions of 973 gene loci were altered overall, with 67 genes shared in SLE and DM, including interferon (IFN) markers\n                      <jats:italic>ISG15<\/jats:italic>\n                      ,\n                      <jats:italic>CXCL10<\/jats:italic>\n                      ,\n                      <jats:italic>OAS1<\/jats:italic>\n                      , and\n                      <jats:italic>STAT1<\/jats:italic>\n                      , and other markers of cell adhesion, immune signaling, and apoptosis. A total of 24 of 32 (75%) pathways were shared in SLE and DM, including granulocyte adhesion, immune cell migration, acute\u2010phase response, apoptosis, and L1CAM signaling. However, SLE peripheral blood exhibited distinctive activation of Type I IFN through increased ligand\u2013receptor interactions not widely elevated in DM. Blood from patients with DM distinctly showed substantially increased expression of intracellular kinases and associated downstream signaling molecules.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Using a multienrichment analytic approach that integrated multiple transcriptomics and proteomics platforms, common underlying immune pathways were identified in SLE and DM. Additionally, two distinctive molecular mechanisms persisted in each condition: IFN signaling was distinctly up\u2010regulated in patients with longstanding SLE, whereas intracellular signaling, particularly kinases, were unique to DM. These shared and distinct findings highlight potential therapeutic opportunities driven by underlying molecular mechanisms.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/acr2.70161","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T14:03:55Z","timestamp":1772978635000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Distinct Interferon and Intracellular Signaling Signatures in Systemic Lupus Erythematosus and Dermatomyositis by Integrative Transcriptomic and Proteomic Analysis"],"prefix":"10.1002","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9510-2848","authenticated-orcid":false,"given":"James M.","family":"Ward","sequence":"first","affiliation":[{"name":"Integrative Bioinformatics Support Group, National Institute of Environmental Health Sciences, NIH, Research Triangle Park  North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7460-7492","authenticated-orcid":false,"given":"Mythri","family":"Ambatipudi","sequence":"additional","affiliation":[{"name":"Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, NIH  Bethesda Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zerai","family":"Manna","sequence":"additional","affiliation":[{"name":"Lupus Clinical Trials Unit, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH  Bethesda Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam","family":"Schiffenbauer","sequence":"additional","affiliation":[{"name":"Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, NIH  Bethesda Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael A.","family":"Smith","sequence":"additional","affiliation":[{"name":"BioPharmaceuticals Research and Development, AstraZeneca  Gaithersburg Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Saifur","family":"Rahman","sequence":"additional","affiliation":[{"name":"BioPharmaceuticals Research and Development, AstraZeneca  Gaithersburg Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2831-9593","authenticated-orcid":false,"given":"Frederick W.","family":"Miller","sequence":"additional","affiliation":[{"name":"Environmental Autoimmunity Group, Clinical Research Branch, National Institute of Environmental Health Sciences, NIH, Research Triangle Park  North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariana J.","family":"Kaplan","sequence":"additional","affiliation":[{"name":"Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland. Dr Smith's current address is Horizon Therapeutics, Gaithersburg, Maryland. Dr Rahman's current address is Sanofi, Cambridge, Massachusetts. Dr Casey's current address is Regeneron Pharmaceuticals  Tarrytown New Jersey"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6487-081X","authenticated-orcid":false,"given":"Jian\u2010Liang","family":"Li","sequence":"additional","affiliation":[{"name":"Integrative Bioinformatics Support Group, National Institute of Environmental Health Sciences, NIH, Research Triangle Park  North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7194-8585","authenticated-orcid":false,"given":"Kerry A.","family":"Casey","sequence":"additional","affiliation":[{"name":"BioPharmaceuticals Research and Development, AstraZeneca  Gaithersburg Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarfaraz","family":"Hasni","sequence":"additional","affiliation":[{"name":"Lupus Clinical Trials Unit, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH  Bethesda 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