{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T11:11:12Z","timestamp":1791803472600,"version":"4.3.4"},"reference-count":24,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2021,11,26]],"date-time":"2021-11-26T00:00:00Z","timestamp":1637884800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2022,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Hidradenitis suppurativa (HS) is a chronic, inflammatory disease of the apocrine gland\u2010rich (AGR) skin region. The initial steps of disease development are not fully understood, despite intense investigations into immune alterations in lesional HS skin.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We aimed to systematically investigate the inflammatory molecules involved in three stages of HS pathogenesis, including healthy AGR, non\u2010lesional HS and lesional HS skin, with the parallel application of multiple mRNA and protein\u2010based methods.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Immune cell counts (T cells, dendritic cells, macrophages), Th1\/Th17\u2010related molecules (IL\u201012B, TBX21, IFNG, TNFA, IL\u201017, IL10, IL\u201023A, TGFB1, RORC, CCL20), keratinocyte\u2010related sensors (TLR2,4), mediators (S100A7, S100A8, S100A9, DEFB4B, LCN2, CAMP, CCL2) and pro\u2010inflammatory molecules (IL1B, IL6, TNFA, IL\u201023A) were investigated in the three groups by RNASeq, RT\u2010qPCR, immunohistochemistry and immunofluorescence.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Epidermal changes were already detectable in non\u2010lesional HS skin; the epidermal occurrence of antimicrobial peptides (AMPs), IL\u20101\u03b2, TNF\u2010\u03b1 and IL\u201023 was highly upregulated compared with healthy AGR skin. In lesional HS epidermis, TNF\u2010\u03b1 and IL\u20101\u03b2 expression remained at high levels while AMPs and IL\u201023 increased even more compared with non\u2010lesional skin. In the dermis of non\u2010lesional HS skin, signs of inflammation were barely detectable (vs. AGR), while in the lesional dermis, the number of inflammatory cells and Th1\/Th17\u2010related mediators were significantly elevated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings that non\u2010lesional HS epidermal keratinocytes produce not only AMPs and IL\u20101\u03b2 but also high levels of TNF\u2010\u03b1 and IL\u201023 confirm the driver role of keratinocytes in HS pathogenesis and highlight the possible role of keratinocytes in the transformation of non\u2010inflammatory Th17 cells (of healthy AGR skin) into inflammatory cells (of HS) via the production of these mediators. The fact that epidermal TNF\u2010\u03b1 and IL\u201023 appear also in non\u2010lesional HS seems to prove these cytokines as excellent therapeutic targets.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jdv.17779","type":"journal-article","created":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T14:33:31Z","timestamp":1635777211000},"page":"462-471","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":42,"title":["Primary alterations during the development of hidradenitis suppurativa"],"prefix":"10.1111","volume":"36","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7787-1002","authenticated-orcid":false,"given":"Z.","family":"Dajnoki","sequence":"first","affiliation":[{"name":"Division of Dermatological Allergology Department of Dermatology Faculty of Medicine University of Debrecen Debrecen Hungary"},{"name":"Department of Dermatology Faculty of Medicine University of Debrecen Debrecen 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