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Using imiquimod and interleukin\u201017A\u2010induced psoriasiform mouse models that exhibited pain\u2010like behaviors, we found that nerve growth factor (NGF) levels were elevated in lesional skin, activating TrkA signaling in dorsal root ganglion neurons and promoting Schwann\u2010cell hypertrophy. Normally, Schwann cells (SCs) limit NGF signaling in cutaneous peripheral nerves through the p75NTR receptor. However, inflammation driven by interleukin\u201017A increased non\u2010muscle myosin II activity and elevated NGF levels, leading to the internalization and degradation of p75NTR. The resulting depletion of p75NTR caused local NGF accumulation, excessive TrkA activation, and heightened pain sensitivity. These findings reveal that psoriatic inflammation converts SCs from protective buffers into drivers of pain, offering a mechanistic explanation for why only some patients experience cutaneous pain in psoriasis.<\/jats:p>","DOI":"10.1002\/advs.202523189","type":"journal-article","created":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T05:56:25Z","timestamp":1775282185000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Depletion of p75NTR in Schwann Cells Driven by Inflammation Mediates Cutaneous Pain in Psoriasis"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3633-8276","authenticated-orcid":false,"given":"Yibo","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Dermatology Shandong Provincial Hospital Affiliated to Shandong First Medical University  Jinan Shandong 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