Evidence map›Paper›PMID 42208526›Full record

ArticleImmunity2026

A longitudinal atlas of human psoriatic skin reveals the mechanisms of anti-IL-23 therapy in disrupting the type 17 inflammatory circuit.

Rundong Jiang, Andrew Blauvelt, Linyu Shi, Lam C Tsoi, Rachael Bogle, Jennifer Fox, Mehrnaz Gharaee-Kermani, Lihong Chen, Haihan Zhang, Xianying Xing and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. CD8Frontiers in immunology · 2026
    Review
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

18 authors.

Rundong JiangDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA; Graduate Program in Immunology, University of Michigan, Ann Arbor, MI, USA; Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan Province, China.
Andrew BlauveltOregon Medical Research Center, Portland, OR, USA.
Linyu ShiAbbVie Inc., North Chicago, IL, USA.
Lam C TsoiDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Rachael BogleDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Jennifer FoxDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Mehrnaz Gharaee-KermaniDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Lihong ChenDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA; Department of Dermatology, Shanghai Jiao Tong University Medical School Affiliated Ruijin Hospital, Shanghai, China.
Haihan ZhangDepartment of Biostatistics, University of Michigan, Ann Arbor, MI, USA.
Xianying XingDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Mrinal K SarkarDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Olesya PlazyoDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
J Michelle KahlenbergDepartment of Internal Medicine, Division of Rheumatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Allison C BilliDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Robert T MathesonOregon Medical Research Center, Portland, OR, USA.
Huzefa PhotowalaAbbVie Inc., North Chicago, IL, USA.
Benjamin D EhstOregon Medical Research Center, Portland, OR, USA.
Johann E GudjonssonDepartment of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA; Department of Internal Medicine, Division of Rheumatology, University of Michigan Medical School, Ann Arbor, MI, USA. Electronic address: johanng@med.umich.edu.

Funding

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
NIAMS NIH HHS P30 AR075043
6 · The paper itself

Abstract

Biologic therapies targeting the IL-23/IL-17 axis have transformed the treatment of psoriasis and show lasting efficacy after treatment cessation. To investigate the immune mechanisms behind these biologics, we performed single-cell RNA sequencing and spatial transcriptomics on matched pre- and post-treatment psoriatic skin samples from patients treated with IL-23 blockade and followed longitudinally for 36 weeks after treatment cessation. IL-23 blockade resulted in a durable reduction in IL-17-producing CD8

Indexed as

Interleukin-17Interleukin-23PsoriasisSkinTh17 CellsCD8-Positive T-LymphocytesDendritic CellsFibroblastsHumansInflammationInterleukin-17Interleukin-23dendritic cellendothelial cellfibroblastIL-23IL-34IL-7Rpsoriasisrisankizumabtissue resident memory TTrm

Identifiers

PMID42208526
PMCPMC13293287

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.