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AA has been recently linked to atopy and shown to exhibit both Th1\u2010 and Th2\u2010driven inflammation. However, a comprehensive molecular and cellular characterization across blood and scalp compartments in both atopic and nonatopic patients is lacking.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Lesional and nonlesional scalp biopsies obtained from AA patients with (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200916) or without (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200920) atopic history, and 17 demographically matched healthy controls were analyzed with RNA\u2010seq, RT\u2010PCR, and immunohistochemistry. Flow cytometry was also performed on peripheral blood mononuclear cells (PBMCs) from a subset of patients. Differential expression was defined using |fold\u2010change|\u2009&gt;\u20091.5 and false\u2010discovery rate &lt;0.05.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      AA scalp exhibited robust upregulation of Th1\u2010 (\n                      <jats:italic>IFNG<\/jats:italic>\n                      ,\n                      <jats:italic>CXCL9<\/jats:italic>\n                      ,\n                      <jats:italic>CXCL10<\/jats:italic>\n                      ,\n                      <jats:italic>CXCL11<\/jats:italic>\n                      ) and Th2\u2010related products (\n                      <jats:italic>CCL26<\/jats:italic>\n                      ,\n                      <jats:italic>CCR4<\/jats:italic>\n                      ,\n                      <jats:italic>IL10<\/jats:italic>\n                      ,\n                      <jats:italic>IL13<\/jats:italic>\n                      ,\n                      <jats:italic>TSLP<\/jats:italic>\n                      ,\n                      <jats:italic>TNFRSF4<\/jats:italic>\n                      \/OX40) and shared downregulation of hair keratins, regardless of atopic background, with variable Th17\/Th22 modulation. AA patients with atopy exhibited greater inflammatory tone and Th2\u2010skewing (\n                      <jats:italic>IL10<\/jats:italic>\n                      ,\n                      <jats:italic>IL13<\/jats:italic>\n                      ,\n                      <jats:italic>IL33<\/jats:italic>\n                      ,\n                      <jats:italic>CCR4<\/jats:italic>\n                      ,\n                      <jats:italic>CCL26<\/jats:italic>\n                      ). Disease severity correlated significantly with immune and hair keratin biomarkers and with perifollicular cellular infiltrates. Cutaneous OX40\/OX40L upregulation was paralleled by increases in circulating OX40\n                      <jats:sup>+<\/jats:sup>\n                      and OX40L\n                      <jats:sup>+<\/jats:sup>\n                      leukocytes, regardless of atopic background.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our results suggest some atopy\u2010associated immune differences in AA and highlight the OX40 axis as a potential novel therapeutic target that may broadly benefit AA patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/all.16268","type":"journal-article","created":{"date-parts":[[2024,8,8]],"date-time":"2024-08-08T09:52:25Z","timestamp":1723110745000},"page":"3401-3414","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Alopecia areata exhibits 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