Evidence map›Paper›PMID 40886965›Full record

ArticleThe Journal of investigative dermatology2026

Spatial and Single-Cell Transcriptomics Reveal Keratinocytes as Key Players in Vulvar Lichen Sclerosus Pathogenesis.

Peng Sun, Christina N Kraus, Wei Zhao, Jiahui Xu, Susie Suh, Quy Nguyen, Yunlong Jia, Arjun Nair, Melanie Oakes, Roberto Tinoco and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. New Insights into the Neglected Disease Vulvar Lichen Sclerosus.The Journal of investigative dermatology · 2026
    Article
  5. Article
  6. Article
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.

Peng SunDepartment of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, California, USA; Department of Dermatology, School of Medicine, University of California, Irvine, Irvine, California, USA.
Christina N KrausDepartment of Dermatology, School of Medicine, University of California, Irvine, Irvine, California, USA. Electronic address: ckraus@hs.uci.edu.
Wei ZhaoDepartment of Mathematics, University of California, Irvine, Irvine, California, USA.
Jiahui XuDepartment of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, California, USA.
Susie SuhDepartment of Dermatology, School of Medicine, University of California, Irvine, Irvine, California, USA.
Quy NguyenDepartment of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, California, USA.
Yunlong JiaDepartment of Developmental and Cell Biology, University of California, Irvine, Irvine, California, USA.
Arjun NairDepartment of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, California, USA.
Melanie OakesDepartment of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, California, USA.
Roberto TinocoDepartment of Molecular Biology and Biochemistry, University of California, Irvine, Irvine, California, USA.
Jessica ShiuDepartment of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, California, USA.
Bryan SunDepartment of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, California, USA; Department of Dermatology, School of Medicine, University of California, Irvine, Irvine, California, USA.
Ashley ElsensohnDepartment of Dermatology, Loma Linda University, Loma Linda, California, USA; Department of Pathology, Loma Linda University, Loma Linda, California, USA.
Scott X AtwoodDepartment of Dermatology, School of Medicine, University of California, Irvine, Irvine, California, USA; Department of Developmental and Cell Biology, University of California, Irvine, Irvine, California, USA.
Qing NieDepartment of Mathematics, University of California, Irvine, Irvine, California, USA; Department of Developmental and Cell Biology, University of California, Irvine, Irvine, California, USA.
Xing DaiDepartment of Biological Chemistry, School of Medicine, University of California, Irvine, Irvine, California, USA; Department of Dermatology, School of Medicine, University of California, Irvine, Irvine, California, USA. Electronic address: xdai@uci.edu.

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Melanie Funes · 1994 to 2026
$57.9M
University of Michigan Skin Biology and Diseases Resource-based CenterP30AR075043 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Johann Eli Gudjonsson · 2019 to 2026
$6.6M
UCI P30 Skin Center Systems Biology CoreP30AR075047 · NIAMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI ANDERSEN, BOGI, GANESAN, ANAND K · 2019 to 2025
$5.1M
Multiscale Models of Wound Cell Plasticity for RegenerationU01AR073159 · NIAMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI DAI, XING, NIE, QING · 2018 to 2022
$3.5M
Intrinsic and extrinsic control of epithelial tissue stem cell activityR35GM145307 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Xing Dai · 2022 to 2026
$2.2M
Development of tools for analyzing cell-cell communication using spatial transcriptomic dataR01GM152494 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Zixuan Cang, Qing Nie · 2024 to 2026
$1.0M
Interdisciplinary Training Program in Skin BiologyT32AR080622 · NIAMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Bogi Andersen, Anand K Ganesan · 2022 to 2026
$909k
NCI NIH HHS P30 CA062203NIAMS NIH HHS P30 AR075043NIAMS NIH HHS P30 AR075047NIAMS NIH HHS T32 AR080622NIAMS NIH HHS U01 AR073159NIGMS NIH HHS R01 GM152494NIGMS NIH HHS R35 GM145307
6 · The paper itself

Abstract

Vulvar diseases are a neglected area of women's health, profoundly affecting patients' QOL. Lichen sclerosus is a chronic inflammatory vulvar skin disorder leading to severe itching, pain, scarring, and an increased risk of malignancy. Despite this burden, the molecular pathogenesis of vulvar lichen sclerosus is not well-understood, limiting treatment options. In this study, we analyze lesional, nonlesional, and healthy vulvar skin using technologies including spatial and single-cell transcriptomics. Our findings identify unifying molecular changes across multiple cell types in lesional vulvar lichen sclerosus skin, including keratinocyte stress response, necroptosis, and basal/stem cell depletion. Chronic T-cell activation, enhanced cytotoxicity, aberrant cell-cell communication, and elevated IFN-γ/JAK/signal transducer and activator of transcription signaling were also observed. Functional studies suggest keratinocytes' dual role as both targets of microenvironmental signaling (eg, IFN-γ) and sources of inflammatory alarmins (eg, S100A8/9). This work reveals keratinocytes as central players in vulvar lichen sclerosus pathogenesis and identifies potential biomarkers and therapeutic targets for future research.

Indexed as

KeratinocytesTranscriptomeVulvar Lichen SclerosusAdultAlarminsCell CommunicationFemaleGene Expression ProfilingHumansInterferon-gammaMiddle AgedSignal TransductionSingle-Cell AnalysisSkinAlarminsInterferon-gammaEpidermal keratinocytesIFN-g/JAK/STATSingle-cell RNA-sequencingT cell cytotoxicityVulvar lichen sclerosus

Identifiers

PMID40886965
PMCPMC12591268

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.