{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T16:16:16Z","timestamp":1791994576541,"version":"4.4.0"},"reference-count":32,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2023,6,12]],"date-time":"2023-06-12T00:00:00Z","timestamp":1686528000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81960564"],"award-info":[{"award-number":["81960564"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82260621"],"award-info":[{"award-number":["82260621"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2023,9]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Pemphigus vulgaris (PV) is a potentially fatal autoimmune bullous disease primarily caused by acantholysis of keratinocytes attributed to pathogenic desmoglein\u20103 (Dsg3) autoantibodies. Interleukin\u201037 (IL\u201037) reportedly plays important roles in a variety of autoimmune diseases, but its role in PV is not clear.<\/jats:p><\/jats:sec><jats:sec><jats:title>Objectives<\/jats:title><jats:p>To investigate whether IL\u201037 plays a role in the occurrence and progression of PV.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>HaCaT keratinocytes were stimulated with anti\u2010Dsg3 antibody to establish an <jats:italic>in vitro<\/jats:italic> PV model, which was defined as anti\u2010Dsg3 group. Cells incubated with medium without anti\u2010Dsg3 treatment were used as control. IL\u201037 was cultured with these cells infected with or without lentiviral vector shRNA\u2010Caveolin\u20101 (sh\u2010Cav\u20101\u2010LV). Cell dissociation assay and immunocytofluorescence were performed to assess keratinocyte dissociation, keratin retraction and Dsg3 endocytosis. Real\u2010time PCR was used to detect the mRNA level of Cav\u20101, and western blot was used to determine the protein expression of Cav\u20101, Dsg3, STAT3 and phosphorylated\u2010STAT3 (p\u2010STAT3).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The anti\u2010Dsg3 group showed more cell debris, increased keratin retraction, increased Dsg3 endocytosis, reduced Cav\u20101 expression and co\u2010localization than the control group, while IL\u201037 treatment neutralized all of these changes. Interestingly, Cav\u20101 knockdown supressed the inhibitory effect of IL\u201037 on keratinocyte dissociation and Dsg3 internalization. The protein expression of p\u2010STAT3 was increased in keratinocytes of the PV model but decreased by IL\u201037. Re\u2010activation of the STAT3 pathway by colivelin supressed the inhibitory effect of IL\u201037 on keratinocyte dissociation and Dsg3 internalization, along with upregulation of Cav\u20101 and Dsg3.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>IL\u201037 inhibited keratinocyte dissociation and Dsg3 endocytosis in an <jats:italic><jats:bold>in vitro<\/jats:bold><\/jats:italic> PV model through the upregulating Cav\u20101 and inhibiting STAT3 pathway.<\/jats:p><\/jats:sec>","DOI":"10.1111\/jdv.19239","type":"journal-article","created":{"date-parts":[[2023,6,1]],"date-time":"2023-06-01T18:23:56Z","timestamp":1685643836000},"page":"1920-1927","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Interleukin\u201037 inhibits desmoglein\u20103 endocytosis and keratinocyte dissociation via upregulation of Caveolin\u20101 and inhibition of the <scp>STAT3<\/scp> 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