ArticleNature communications2025
Serotonin 2A receptor attenuates psoriatic inflammation by suppressing IL-23 secretion in monocyte-derived Langerhans cells.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Pretreatment with the psychedelic DOI mitigates LPS-induced hippocampal inflammation and behavioral impairments in mice.BMC neuroscience · 2026Article
- Animal Assisted Activities (AAAs) with Dogs in a Dialysis Center in Southern Italy: Evaluation of Serotonin and Oxytocin Values in Involved Patients.Biomedicines · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
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 the non-canonical NFκB pathway. Serotonin is the putative agonist modulating HTR2A, attenuating psoriatic inflammation. Lastly, our findings in mice are also validated clinically. Our data demonstrate that serotonin modulates HTR2A, attenuating psoriatic inflammation by suppressing IL-23 secretion via inhibiting the non-canonical NFκB pathway in moLCs.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.