Evidence map›Paper›PMID 41181147›Full record

ArticleFrontiers in immunology2025

Sulfotransferase SULT2B1 contributes to the epithelial-immune microenvironment homeostasis in imiquimod-induced psoriatic dermatitis.

Kenji Morino, Sayaka Akiyoshi, Keisuke Matsubara, Yuki Sugiura, Yoshihiro Izumi, Shu Yotsumoto, Kazuhiko Yamamura, Rae Maeda, Masatomo Takahashi, Keisuke Nakata and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors.

Kenji MorinoDivision of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Sayaka AkiyoshiDivision of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Keisuke MatsubaraDivision of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Yuki SugiuraMultiomics Platform, Center for Cancer Immunotherapy and Immunobiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Yoshihiro IzumiDivision of Metabolomics, Medical Research Center for High Depth Omics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Shu YotsumotoDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kazuhiko YamamuraDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Rae MaedaMultiomics Platform, Center for Cancer Immunotherapy and Immunobiology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Masatomo TakahashiDivision of Metabolomics, Medical Research Center for High Depth Omics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Keisuke NakataDivision of Metabolomics, Medical Research Center for High Depth Omics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Takeshi BambaDivision of Metabolomics, Medical Research Center for High Depth Omics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Takeshi NakaharaDepartment of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Daiji SakataDepartment of Immunology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan.
Takehito UrunoDivision of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Yoshinori FukuiDivision of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Kazufumi KunimuraDivision of Immunogenetics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Skin protects the body from external threats by constituting an epithelial-immune microenvironment. Sulfotransferase family 2B member 1 (SULT2B1) converts cholesterol to cholesterol sulfate (CS). We previously reported that CS acts as an endogenous dedicator of cytokinesis 2 (DOCK2)-inhibitory metabolite suppressing immune cell migration and activation by inhibiting DOCK2-mediated Rac activation. Despite being located in the epidermis, pathophysiological roles of CS in cutaneous inflammation remain unknown. Methods: We evaluated the Results: Discussion: These findings suggest that increased SULT2B1 levels in the skin under psoriatic conditions may be involved in a negative feedback mechanism that helps to limit excessive skin inflammation, thereby potentially contributing to the maintenance of epithelial-immune microenvironment homeostasis. Overall, our results raise the possibility that SULT2B1 plays an important role in cutaneous inflammation and could serve as a useful indicator or potential target in psoriasis.

Indexed as

Cellular MicroenvironmentPsoriasisSulfotransferasesAnimalsCholesterol EstersDisease Models, AnimalFemaleGuanine Nucleotide Exchange FactorsHomeostasisHumansImiquimodKeratinocytesMaleMiceMice, Inbred C57BLMice, KnockoutCholesterol Esterscholesteryl sulfateGuanine Nucleotide Exchange FactorsImiquimodSulfotransferasesSULT2B1b protein, mouseSULT2B1 protein, humancholesterol sulfateDOCK2neutrophilspsoriasisskin inflammationSULT2B1

Identifiers

PMID41181147
PMCPMC12575227

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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.