{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T12:03:28Z","timestamp":1790337808324,"version":"4.1.0"},"reference-count":28,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T00:00:00Z","timestamp":1790208000000},"content-version":"vor","delay-in-days":23,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T00:00:00Z","timestamp":1788220800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100023331","name":"LEO Pharma","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100023331","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100004339","name":"Sanofi","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100004339","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["409525714"],"award-info":[{"award-number":["409525714"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical &amp;amp; Translational All"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Atopic dermatitis (AD) is a chronic inflammatory disease driven by Type 2 (Th2) inflammation. Dupilumab (anti\u2010IL\u20104R\u03b1) and tralokinumab (anti\u2010IL\u201013) are effective biologic therapies, but a direct comparison of their longitudinal effects on the systemic proteome is lacking. This exploratory study aimed to identify and to differentially analyze the proteomic signatures in AD patients treated with dupilumab versus tralokinumab.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In this prospective, observational study, serum samples were collected from patients with moderate\u2010to\u2010severe AD at baseline and after 12\u00a0months of treatment with either dupilumab (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a010) or tralokinumab (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a010). A cohort of healthy controls (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a012) was included for baseline comparison. Proteomic profiling was performed using a targeted 440\u2010protein array, and data were analyzed for differential expression and pathway enrichment.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>At baseline, AD patients exhibited a distinct proteomic signature compared to healthy controls, characterized by a strong Th2 inflammatory profile and enrichment of the IL\u20104\/IL\u201013 signaling pathway. After 12\u00a0months, both therapies reduced the core Th2 inflammatory signature with downregulation of key markers like CCL17. Dupilumab induced a broader immunomodulation, showing a more pronounced upregulation of Th1 associated proteins compared to tralokinumab. Furthermore, the therapies had opposing effects on tissue repair and metabolic proteins; dupilumab treatment led to a decrease in TNFSF11 and Sclerostin (SOST), while these were increased after tralokinumab treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Dupilumab and tralokinumab effectively target the Th2 axis in AD but their longitudinal systemic immune modulation differs in respect to Th1\u2010Th17 and tissue repair markers.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/clt2.70203","type":"journal-article","created":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T02:53:07Z","timestamp":1790304787000},"source":"Crossref","is-referenced-by-count":0,"title":["Longitudinal Proteomic Signatures of Dupilumab and Tralokinumab Treated Atopic Dermatitis Patients"],"prefix":"10.1002","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5361-9876","authenticated-orcid":false,"given":"Wojciech","family":"Francuzik","sequence":"first","affiliation":[{"name":"Division of Allergy and Immunology Department of Dermatology, Venereology and Allergology Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin Corporate Member of Freie Universit\u00e4t Berlin and Humboldt\u2010Universit\u00e4t zu Berlin  Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3959-6986","authenticated-orcid":false,"given":"Kristijan","family":"Pa\u017eur","sequence":"additional","affiliation":[{"name":"Division of Allergy and Immunology Department of Dermatology, Venereology and Allergology Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin Corporate Member of Freie Universit\u00e4t Berlin and Humboldt\u2010Universit\u00e4t zu Berlin  Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3449-1245","authenticated-orcid":false,"given":"Margitta","family":"Worm","sequence":"additional","affiliation":[{"name":"Division of Allergy and Immunology Department of Dermatology, Venereology and Allergology Charit\u00e9\u2014Universit\u00e4tsmedizin Berlin Corporate Member of Freie Universit\u00e4t Berlin and Humboldt\u2010Universit\u00e4t zu Berlin  Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,9,24]]},"reference":[{"key":"e_1_2_13_2_1","doi-asserted-by":"publisher","DOI":"10.2500\/aap.2019.40.4202"},{"key":"e_1_2_13_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s40257\u2010024\u201000856\u20101"},{"key":"e_1_2_13_4_1","doi-asserted-by":"publisher","DOI":"10.3390\/jcm10112506"},{"key":"e_1_2_13_5_1","doi-asserted-by":"publisher","DOI":"10.1002\/cia2.12033"},{"key":"e_1_2_13_6_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1610020"},{"key":"e_1_2_13_7_1","doi-asserted-by":"publisher","DOI":"10.1001\/jamadermatol.2023.0627"},{"key":"e_1_2_13_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2018.10.032"},{"key":"e_1_2_13_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2018.08.022"},{"key":"e_1_2_13_10_1","doi-asserted-by":"publisher","DOI":"10.2147\/JAA.S385645"},{"key":"e_1_2_13_11_1","doi-asserted-by":"publisher","DOI":"10.1111\/cea.13954"},{"key":"e_1_2_13_12_1","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.immunol.17.1.701"},{"key":"e_1_2_13_13_1","doi-asserted-by":"publisher","DOI":"10.3109\/08830189809084486"},{"key":"e_1_2_13_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jmb.2016.12.005"},{"key":"e_1_2_13_15_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrrheum.2015.167"},{"key":"e_1_2_13_16_1","doi-asserted-by":"publisher","DOI":"10.1111\/cea.13495"},{"key":"e_1_2_13_17_1","doi-asserted-by":"publisher","DOI":"10.3389\/fendo.2023.1150222"},{"key":"e_1_2_13_18_1","doi-asserted-by":"publisher","DOI":"10.1111\/1440\u20101681.13103"},{"key":"e_1_2_13_19_1","doi-asserted-by":"publisher","DOI":"10.1002\/art.34649"},{"key":"e_1_2_13_20_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jdcr.2021.12.011"},{"issue":"5","key":"e_1_2_13_21_1","first-page":"16","article-title":"Tralokinumab as a Therapeutic Alternative for Dupilumab\u2010Associated Arthralgia in Atopic Dermatitis: A Multi\u2010Center Case Series","volume":"18","author":"Greenberg A. 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