{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T08:23:16Z","timestamp":1791015796617,"version":"4.1.0"},"reference-count":31,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2023,12,12]],"date-time":"2023-12-12T00:00:00Z","timestamp":1702339200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2024,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Pruritus is a highly burdensome symptom in patients with epidermolysis bullosa, especially recessive dystrophic epidermolysis bullosa (RDEB); however, only a few studies have assessed the molecular pathogenesis of RDEB\u2010associated pruritus. Interleukin (IL)\u201031 is a key cytokine implicated in pruritus associated with dermatologic diseases such as atopic dermatitis and prurigo nodularis.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objective<\/jats:title><jats:p>To investigate the role and cellular source of IL\u201031 in RDEB\u2010associated pruritus.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Serum and skin samples were obtained from 11 RDEB patients and 11 healthy controls. Pruritus visual analogue scale scores were determined. Serum levels of IL\u201031 and thymic stromal lymphopoietin (TSLP) were examined by enzyme\u2010linked immunosorbent assay (ELISA). The expression of IL\u201031 and other pruritus mediators in the skin were examined through immunofluorescence staining, and their correlation with pruritus severity was analysed.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Serum IL\u201031 and TSLP were elevated in RDEB patients. IL\u201031 expression was increased in RDEB skin and positively correlated with pruritus severity. Most of the IL\u201031\u2010expressing cells were mast cells, and some were CD206(+) M2\u2010like macrophages. The number of substance P(+) cells was also increased in the patients' skin, and most of them were mast cells. The number of substance P(+) mast cells was correlated with the number of IL\u201031(+) dermal infiltrates. The number of IL\u20104R\u03b1\u2010 and IL\u201013\u2010expressing cells and expression of TSLP and periostin increased in RDEB skin, but without a correlation to pruritus score.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>The increased production of skin IL\u201031 from mast cells and M2\u2010like macrophages may be the mechanism underlying pruritus in RDEB.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jdv.19738","type":"journal-article","created":{"date-parts":[[2023,12,12]],"date-time":"2023-12-12T23:54:10Z","timestamp":1702425250000},"page":"895-903","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Mechanism underlying pruritus in recessive dystrophic epidermolysis bullosa: Role of interleukin\u201031 from mast cells and macrophages"],"prefix":"10.1111","volume":"38","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6455-8888","authenticated-orcid":false,"given":"Sang 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