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Here, we identify cannabinoid 1 receptor (CB1R) in macrophages as a key immunometabolic regulator of psoriatic inflammation and a potential therapeutic target. CB1R expression was increased in macrophages infiltrating psoriatic lesional skin in both humans and mice, and both pharmacological inhibition and genetic deletion of CB1R markedly attenuated psoriasis\u2010like pathology in mouse models by reducing epidermal hyperplasia, inflammation, and barrier dysfunction in a macrophage\u2010dependent manner. Mechanistically, CB1R signaling in macrophages suppressed expression of the RNA\u2010binding protein AUF1, leading to stabilization of\n                    <jats:italic>Nlrp3<\/jats:italic>\n                    mRNA and enhanced NLRP3 inflammasome activation. AUF1 directly bound an AU\u2010rich region within the\n                    <jats:italic>Nlrp3<\/jats:italic>\n                    3\u2032 untranslated region and promoted mRNA destabilization, thereby limiting inflammasome activation and IL\u20101\u03b2 production. Restoration of AUF1 expression, either by CB1R inhibition or overexpression, reduced NLRP3 levels and alleviated psoriasis\u2010like pathology, whereas\n                    <jats:italic>Nlrp3<\/jats:italic>\n                    deficiency abrogated these effects. Collectively, these findings define a CB1R\u2013AUF1\u2013NLRP3 signaling axis that links metabolic signaling to inflammasome\u2010driven skin inflammation in macrophages. Targeting macrophage CB1R may therefore represent a promising therapeutic strategy for psoriasis and other immunometabolic inflammatory diseases.\n                  <\/jats:p>","DOI":"10.1002\/advs.78313","type":"journal-article","created":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T04:02:56Z","timestamp":1792036976000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Targeting Cannabinoid 1 Receptor in Macrophages Alleviates Psoriatic Skin Inflammation Through the AUF1\u2013NLRP3 Axis"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4639-5995","authenticated-orcid":false,"given":"Hongseo","family":"Choi","sequence":"first","affiliation":[{"name":"Department of Molecular Science &amp; Technology Ajou University  Suwon Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-0284-7093","authenticated-orcid":false,"given":"Sukyoung","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Medical Science, Graduate School The Catholic University of Korea  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jinho","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Life Science Chung\u2010Ang University  Seoul Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-7204-8682","authenticated-orcid":false,"given":"Ji Hye","family":"Han","sequence":"additional","affiliation":[{"name":"Department of Molecular Science &amp; 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