ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Tm4sf19 inhibition alleviates imiquimod-induced psoriatic dermatitis by regulating inflammatory signaling pathways and keratinocyte proliferation in mice.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPsoriasis is a chronic inflammatory disease characterized by keratinocyte hyperproliferation, immune cell infiltration, and persistent inflammatory signaling. Although Tm4sf19 has been implicated in inflammatory processes, its contribution to psoriasis pathogenesis remains unclear.
methodsWe investigate the role of Tm4sf19 in psoriatic inflammation was examined using an imiquimod-induced psoriasis mouse model and HaCaT keratinocytes, in which Tm4sf19 expression was deleted genetically or suppressed pharmacologically with the competitive inhibitor, LEL-Fc. Gene expression, protein expression, and tissue changes were assessed by qPCR, western blotting and histological scoring, respectively.
resultsTm4sf19 expression was significantly elevated in psoriatic lesion. Tm4sf19 knockout or inhibition using LEL-Fc suppressed psoriatic symptoms, macrophage-mediated inflammation and inflammatory cytokine expression. Tm4sf19 inhibition also suppressed the activation of STAT3, EGFR, ERK and KRT17 signaling pathways in keratinocytes. Furthermore, LEL-Fc treatment effectively inhibited LPS-induced cell cycle progression and promoted apoptosis in keratinocyte both in vivo and in vitro.
conclusionThese findings suggest that Tm4sf19 regulates psoriatic inflammation and keratinocyte proliferation through major signaling pathways. Therefore, inhibiting Tm4sf19 may have therapeutic potential for the treatment of psoriasis.
Indexed as
Identifiers
41998341What 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.