{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,12]],"date-time":"2026-06-12T18:18:21Z","timestamp":1781288301235,"version":"3.54.1"},"reference-count":79,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2024,10,4]],"date-time":"2024-10-04T00:00:00Z","timestamp":1728000000000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"funder":[{"DOI":"10.13039\/100007475","name":"Canadian Dermatology Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100007475","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2024,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Stress may play a key role in alopecia areata (AA), though the exact interactions of stress with AA remain undefined. Corticotropin\u2010releasing hormone (CRH), the proximal regulator of the stress axis, has been recognized as an immunomodulatory factor in tissues and peripheral blood mononuclear cells (PBMCs). We used multicolour flow cytometry to identify receptor CRHR1 expression on PBMC subsets in AA patients (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200954) and controls (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200966). We found that CRHR1 was primarily expressed by circulating monocytes. CRHR1 expression on monocytes was enhanced in AA compared with controls (3.17% vs. 1.44%,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.002, chi\u2010squared test). AA incidence was correlated to elevated CD14\n                    <jats:sup>+<\/jats:sup>\n                    monocyte numbers (\n                    <jats:italic>R<\/jats:italic>\n                    \u2009=\u20090.092,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.036) and markedly independently correlated with increased CRHR1 expression (\n                    <jats:italic>R<\/jats:italic>\n                    \u2009=\u20090.215,\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.027). High CRHR1 expression was significantly related to chronic AA (disease duration &gt;1\u2009year;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.003, chi\u2010squared test), and large lesion area (AA area &gt;25%;\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.049, chi\u2010squared test). We also observed enhanced percentages of active monocytes and reduced CD16\n                    <jats:sup>+<\/jats:sup>\n                    \u2009CD3\u2212 NK cell numbers in AA patients' PBMCs (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.010; 0.025, respectively). In\u00a0vitro CRH treatment of PBMCs and human monocyte cell line THP\u20101 promoted CD86 upregulation. The findings imply that stress\u2010related factors CRH and CRHR1 contribute to AA development and progression where higher CRHR1 expression is associated with chronic AA and larger lesions.\n                  <\/jats:p>","DOI":"10.1111\/exd.15182","type":"journal-article","created":{"date-parts":[[2024,10,5]],"date-time":"2024-10-05T00:55:08Z","timestamp":1728089708000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Increased\n                    <scp>CRHR1<\/scp>\n                    expression on monocytes from patients with\n                    <scp>AA<\/scp>\n                    enables a pro\u2010inflammatory response to corticotrophin\u2010releasing hormone"],"prefix":"10.1111","volume":"33","author":[{"given":"Hong\u2010Wei","family":"Guo","sequence":"first","affiliation":[{"name":"Department of Dermatology and Skin Science University of British Columbia  Vancouver British Columbia Canada"},{"name":"Department of Dermatology The Second Affiliated Hospital of Guangdong Medical University  Zhanjiang Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2136-8627","authenticated-orcid":false,"given":"Hui\u2010Jun","family":"Lai","sequence":"additional","affiliation":[{"name":"Department of Dermatology The Second Affiliated Hospital of Guangdong Medical University  Zhanjiang Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo\u2010Quan","family":"Long","sequence":"additional","affiliation":[{"name":"Department of Dermatology The Second Affiliated Hospital of Guangdong Medical University  Zhanjiang Guangdong China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li\u2010Xin","family":"Xu","sequence":"additional","affiliation":[{"name":"Flow Core Facility Children and Family Research Institute  Vancouver British Columbia Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eddy Hsi Chun","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Skin Science University of British Columbia  Vancouver British Columbia Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jerry","family":"Shapiro","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Skin Science University of British Columbia  Vancouver British Columbia Canada"},{"name":"The Ronald O. Perelman Department of Dermatology New York University Grossman School of Medicine  New York New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kevin J.","family":"McElwee","sequence":"additional","affiliation":[{"name":"Department of Dermatology and Skin Science University of British Columbia  Vancouver British Columbia Canada"},{"name":"Centre for Skin Sciences University of Bradford  Bradford West Yorkshire 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