{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tan YF"],"funding":["National Taiwan University Hospital","National Taiwan University Hospital (NTUH)","Academia Sinica"],"pagination":["8544"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12480967"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Anecdotal evidence has suggested an association between psychiatric drugs and psoriasis, but consensus is absent due to contradicting reports, and the mechanism remains poorly defined. Here, we investigate the function of serotonin 2A receptor (HTR2A), a receptor commonly targeted by psychiatric drugs, in regulating psoriasis. HTR2A antagonistic drugs worsen psoriatic outcome, and HTR2A modulation reduces psoriatic inflammation. Using the Imiquimod-induced psoriasiform model, HTR2A-deficient mice manifest exacerbated inflammation. Hematopoietic cells, particularly monocyte-derived Langerhans cells (moLC), are involved in this phenotype. Mechanistically, the exacerbated inflammation is due to increased interleukin-23 (IL-23) secretion, and HTR2A suppresses this by inhibiting activation of t"],"journal":["Nature communications"],"pubmed_title":["Serotonin 2A receptor attenuates psoriatic inflammation by suppressing IL-23 secretion in monocyte-derived Langerhans cells."],"pmcid":["PMC12480967"],"funding_grant_id":["AS-IDR-112-01","UN110-032","AS-BRPT-112-01","UN108-015"],"pubmed_authors":["Tsai CH","Yeh CY","Tsai TF","Lu CH","Chiang PC","Lee YL","Hsu SY","Tan YF","Weng HJ"],"additional_accession":[]},"is_claimable":false,"name":"Serotonin 2A receptor attenuates psoriatic inflammation by suppressing IL-23 secretion in monocyte-derived Langerhans cells.","description":"Anecdotal evidence has suggested an association between psychiatric drugs and psoriasis, but consensus is absent due to contradicting reports, and the mechanism remains poorly defined. Here, we investigate the function of serotonin 2A receptor (HTR2A), a receptor commonly targeted by psychiatric drugs, in regulating psoriasis. HTR2A antagonistic drugs worsen psoriatic outcome, and HTR2A modulation reduces psoriatic inflammation. Using the Imiquimod-induced psoriasiform model, HTR2A-deficient mice manifest exacerbated inflammation. Hematopoietic cells, particularly monocyte-derived Langerhans cells (moLC), are involved in this phenotype. Mechanistically, the exacerbated inflammation is due to increased interleukin-23 (IL-23) secretion, and HTR2A suppresses this by inhibiting activation of t","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-07-15T09:47:30.693Z","creation":"2026-07-02T03:12:39.129Z"},"accession":"S-EPMC12480967","cross_references":{"pubmed":["41022781"],"doi":["10.1038/s41467-025-63971-5"]}}