{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T22:27:52Z","timestamp":1789079272166,"version":"build-2803163510"},"reference-count":143,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,11,17]],"date-time":"2025-11-17T00:00:00Z","timestamp":1763337600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,11,17]],"date-time":"2025-11-17T00:00:00Z","timestamp":1763337600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100004319","name":"Pfizer","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004319","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2026,2]]},"abstract":"ABSTRACT<\/jats:title>\n \n Background<\/jats:title>\n While significant progress has been made in understanding the molecular characteristics of inflammatory skin diseases, their systemic impact warrants further investigation. A comprehensive large\u2010scale study that examines systemic proteomic expression across the most common inflammatory skin diseases is currently lacking.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Serum from 38 alopecia areata\/\n AA<\/jats:styled-content>\n , 41 atopic dermatitis\/\n AD<\/jats:styled-content>\n , 21 psoriasis, 18 hidradenitis suppurativa\/\n HS<\/jats:styled-content>\n , and 25 vitiligo patients was analyzed using\n OLINK<\/jats:styled-content>\n high\u2010throughput multiplex assay explore panel and compared to 49 healthy\u2010matched controls. Differentially expressed proteins\/\n DEPs<\/jats:styled-content>\n were defined using the criteria of fold change\/|\n FCH<\/jats:styled-content>\n |\u2009>\u20091.2,\n FDR\u2009<<\/jats:styled-content>\n \u20090.1. Spearman analysis was also conducted to identify correlations between biomarkers and disease severity. Gene ontology of\n DEPs<\/jats:styled-content>\n was performed using enrichr.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Our results reveal both distinct and shared patterns of systemic dysregulation across the spectrum of inflammatory diseases.\n HS<\/jats:styled-content>\n exhibited the highest level of dysregulation compared to healthy serum, followed by\n AA<\/jats:styled-content>\n ,\n AD<\/jats:styled-content>\n , psoriasis, and vitiligo. The\n DEPs<\/jats:styled-content>\n identified in\n HS<\/jats:styled-content>\n showed the greatest overlap with those in psoriasis, while\n AA<\/jats:styled-content>\n and\n AD<\/jats:styled-content>\n also displayed significant similarity.\n HS<\/jats:styled-content>\n and\/or psoriasis primarily showed upregulation of markers belonging to T\u2010cell activation\/migration (interleukin\/\n IL<\/jats:styled-content>\n \u2010\n 2RA<\/jats:styled-content>\n \/\n CD40LG<\/jats:styled-content>\n ), innate immunity (\n IL<\/jats:styled-content>\n \u20106\/\n CXCL8<\/jats:styled-content>\n \/\n IL<\/jats:styled-content>\n \u20108), Th1 (\n TNF<\/jats:styled-content>\n \/\n CXCL9<\/jats:styled-content>\n \/\n CXCL10<\/jats:styled-content>\n ), and Th17\/22 (\n IL<\/jats:styled-content>\n \u2010\n 17A<\/jats:styled-content>\n \/\n IL<\/jats:styled-content>\n \u201020\/\n CXCL1<\/jats:styled-content>\n \/\n LCN2<\/jats:styled-content>\n ) compared to normal.\n AA<\/jats:styled-content>\n and\/or\n AD<\/jats:styled-content>\n were characterized by upregulation of markers of general inflammation (\n MMP12<\/jats:styled-content>\n ), T\u2010cell activation\/migration (\n IL<\/jats:styled-content>\n \u201015\/\n IL<\/jats:styled-content>\n \u201016), T Helper 1\/Th1 (\n IFNGR1<\/jats:styled-content>\n \/\n CXCL10<\/jats:styled-content>\n ), Th2 (\n IL<\/jats:styled-content>\n \u2010\n 4R<\/jats:styled-content>\n \/\n CCL26<\/jats:styled-content>\n \/\n CCL27<\/jats:styled-content>\n ), Th17\/22 (\n IL<\/jats:styled-content>\n \u201019\/\n IL<\/jats:styled-content>\n \u201020\/\n PI3<\/jats:styled-content>\n ) compared to controls.\n HS<\/jats:styled-content>\n showed the largest dysregulation in cardiovascular\/\n CV<\/jats:styled-content>\n \/atherosclerosis markers (\n PDGFA<\/jats:styled-content>\n \/\n SELP<\/jats:styled-content>\n \/\n MMP9<\/jats:styled-content>\n ) compared to controls (all\n FDR\u2009<<\/jats:styled-content>\n \u20090.05). Spearman analysis captured multiple positive correlations between key immune markers (\n IL<\/jats:styled-content>\n \u2010\n 4R<\/jats:styled-content>\n \/\n OX40<\/jats:styled-content>\n \/\n TNFRSF4<\/jats:styled-content>\n \/\n IL<\/jats:styled-content>\n \u2010\n 17A<\/jats:styled-content>\n \/\n TNF<\/jats:styled-content>\n ) and respective clinical severity scores (e.g.,\n SALT<\/jats:styled-content>\n ,\n SCORAD<\/jats:styled-content>\n ,\n IHS4<\/jats:styled-content>\n ,\n PASI<\/jats:styled-content>\n ).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n Various inflammatory skin diseases show shared and distinct systemic protein immune activation. Overlap across conditions encourages the investigation of shared therapeutic approaches.<\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/all.70157","type":"journal-article","created":{"date-parts":[[2025,11,17]],"date-time":"2025-11-17T11:20:52Z","timestamp":1763378452000},"page":"524-538","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Large\u2010Scale Blood Proteomic Analysis Across Different Inflammatory Skin Conditions Reveals Extensive Immune Dysregulation With Distinct Biomarker Profiles"],"prefix":"10.1111","volume":"81","author":[{"given":"Jacob W.","family":"Glickman","sequence":"first","affiliation":[{"name":"Department of Dermatology and Laboratory of Inflammatory Skin Diseases Icahn School of Medicine at Mount Sinai New York New York 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