{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T23:10:33Z","timestamp":1773011433450,"version":"3.50.1"},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,2,12]],"date-time":"2026-02-12T00:00:00Z","timestamp":1770854400000},"content-version":"vor","delay-in-days":11,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T00:00:00Z","timestamp":1769904000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82071832"],"award-info":[{"award-number":["82071832"]}],"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":["81772909"],"award-info":[{"award-number":["81772909"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunity Inflam &amp;amp; Disease"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Psoriasis, a common chronic inflammatory skin disease, is characterized by epidermal hyperplasia and inflammatory cell infiltration. While endosomal Toll\u2010like receptors (TLRs), particularly TLR7, are key drivers of psoriatic exacerbations, the regulatory mechanisms governing TLR7 activity in psoriasis remain incompletely understood. This study aims to investigate the role of G protein\u2010coupled receptor 108 (GPR108) in regulating TLR7 activity during imiquimod (IMQ)\u2010induced psoriasiform dermatitis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We established IMQ\u2010induced psoriasiform lesions in\n                      <jats:italic>Gpr108<\/jats:italic>\n                      \u2010null mice, as well as IMQ\u2010treated GPR108\u2010deficient keratinocyte and macrophage models. The psoriasis\u2010like phenotype was assessed in vivo using PASI scoring and H&amp;E staining. Protein expression was examined by Western blotting, immunohistochemistry, and immunofluorescence. Additionally, RNA\u2010seq and flow cytometric analyses were performed to verify the involvement of the TLR7\/NF\u2010\u03baB signaling in regulating GPR108\u2010deficient macrophage polarization.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We found that\n                      <jats:italic>Gpr108<\/jats:italic>\n                      deficiency exacerbates IMQ\u2010induced psoriatic lesions in mice. Mechanistically, GPR108 deficiency enhances TLR7\/MyD88\/NF\u2010\u03baB signaling in both keratinocytes and macrophages following imiquimod stimulation. This increased TLR7 activation promotes keratinocyte hyperproliferation and dysregulated differentiation, and alters the M1\/M2 macrophage balance, leading to elevated production of cytokines, including TNF\u2010\u03b1 and IL\u20106.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>GPR108 functions as a negative regulator of TLR7 signaling in psoriasis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/iid3.70346","type":"journal-article","created":{"date-parts":[[2026,2,13]],"date-time":"2026-02-13T06:41:44Z","timestamp":1770964904000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["GPR108 Negatively Regulates TLR7 Signaling in Imiquimod\u2010Induced Psoriasiform Dermatitis"],"prefix":"10.1002","volume":"14","author":[{"given":"Wenwen","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Anhui Medical University Hefei China"},{"name":"Clinical Laboratory Mianyang Maternity and Child Healthcare Hospital Mianyang China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuyan","family":"Zhang","sequence":"additional","affiliation":[{"name":"Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education Hefei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kainan","family":"Liao","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Anhui Medical University Hefei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Qiantong","family":"Xiang","sequence":"additional","affiliation":[{"name":"Department of Dermatology The Affiliated Hefei Hospital of Anhui Medical University Hefei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Dandan","family":"Zang","sequence":"additional","affiliation":[{"name":"Center for Scientific Research Anhui Medical University Hefei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chunlin","family":"Cai","sequence":"additional","affiliation":[{"name":"Department of Pathophysiology School of Basic Medical Sciences, Anhui Medical University Hefei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4195-2801","authenticated-orcid":false,"given":"Fusheng","family":"Zhou","sequence":"additional","affiliation":[{"name":"Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education Hefei China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Haisheng","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology Anhui Medical University Hefei China"},{"name":"Key Laboratory of Dermatology (Anhui Medical University), Ministry of Education Hefei China"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2026,2,12]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.3389\/fimmu.2022.941071"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/JLB.5MR0120-439R"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.3389\/fmolb.2023.1201912"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms21207488"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1468-3083.2011.04049.x"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.3390\/ijms20184347"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.3390\/molecules24112157"},{"key":"e_1_2_10_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaad.2005.10.057"},{"key":"e_1_2_10_10_1","doi-asserted-by":"publisher","DOI":"10.1038\/emm.2017.81"},{"key":"e_1_2_10_11_1","doi-asserted-by":"publisher","DOI":"10.1080\/10425170701207182"},{"key":"e_1_2_10_12_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.omtm.2020.03.012"},{"key":"e_1_2_10_13_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0205303"},{"key":"e_1_2_10_14_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.intimp.2017.04.022"},{"key":"e_1_2_10_15_1","doi-asserted-by":"publisher","DOI":"10.1002\/iid3.1104"},{"key":"e_1_2_10_16_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ymthe.2019.11.005"},{"key":"e_1_2_10_17_1","doi-asserted-by":"publisher","DOI":"10.1186\/gb-2007-8-6-r104"},{"key":"e_1_2_10_18_1","first-page":"52","article-title":"Going, Toll\u2010Like Receptors in Skin Inflammation and Inflammatory Diseases","volume":"20","author":"Kumar V.","year":"2021","journal-title":"EXCLI Journal"},{"key":"e_1_2_10_19_1","first-page":"1","article-title":"Involvement of M1 Macrophage Polarization in Endosomal Toll\u2010Like Receptors Activated Psoriatic Inflammation","volume":"2018","author":"Lu C. 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