Evidence map›Paper›PMID 40516577›Full record

ArticleThe Journal of allergy and clinical immunology2025

Positionally distinct interferon-stimulated dermal immune-acting fibroblasts promote neutrophil recruitment in Sweet syndrome.

Kellen J Cavagnero, Julie Albright, Fengwu Li, Edward Liu, Tatsuya Dokoshi, Rachael Bogle, Joseph Kirma, J Michelle Kahlenberg, Allison C Billi, Jennifer Fox and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of allergy and clinical immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Sweet Syndrome Beyond the Neutrophil.Experimental dermatology · 2026
    Article
  2. Fibroblasts resistScience advances · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Kellen J CavagneroDepartment of Dermatology, University of California San Diego, La Jolla, Calif.
Julie AlbrightDepartment of Dermatology, University of California San Diego, La Jolla, Calif.
Fengwu LiDepartment of Dermatology, University of California San Diego, La Jolla, Calif.
Edward LiuDepartment of Dermatology, University of California San Diego, La Jolla, Calif.
Tatsuya DokoshiDepartment of Dermatology, University of California San Diego, La Jolla, Calif.
Rachael BogleDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
Joseph KirmaDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
J Michelle KahlenbergDepartment of Dermatology, University of Michigan, Ann Arbor, Mich; Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich; Taubman Medical Research Institute, Ann Arbor, Mich.
Allison C BilliDepartment of Dermatology, University of Michigan, Ann Arbor, Mich; Taubman Medical Research Institute, Ann Arbor, Mich.
Jennifer FoxDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
May P ChanDepartment of Pathology, University of Michigan, Ann Arbor, Mich.
Anthony CoonDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
Craig J DobryDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
Brian HindsDepartment of Dermatology, University of California San Diego, La Jolla, Calif.
Lam C TsoiDepartment of Dermatology, University of Michigan, Ann Arbor, Mich.
Paul W HarmsDepartment of Dermatology, University of Michigan, Ann Arbor, Mich; Department of Pathology, University of Michigan, Ann Arbor, Mich.
Johann E GudjonssonDepartment of Dermatology, University of Michigan, Ann Arbor, Mich; Division of Rheumatology, Department of Internal Medicine, University of Michigan, Ann Arbor, Mich; Taubman Medical Research Institute, Ann Arbor, Mich.
Richard L GalloDepartment of Dermatology, University of California San Diego, La Jolla, Calif. Electronic address: rgallo@health.ucsd.edu.

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Alexey I Nesvizhskii · 1988 to 2026
$178.2M
Microbiology and Metagenomics CoreP50AR080594 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROBERT L MODLIN · 2022 to 2026
$9.2M
Training Grant in GastroenterologyT32DK007202 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GHOSH, PRADIPTA · 1985 to 2022
$7.7M
Skin microbes and development of allergic diseaseR01AI192662 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GALLO, RICHARD L, KNIGHT, ROB · 2025 to 2025
$5.2M
Cathelicidin in Skin ImmunityR37AI052453 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard L Gallo, Victor Nizet · 2019 to 2026
$4.6M
Microbiome Function in Atopic DermatitisU01AI152038 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard L Gallo · 2020 to 2026
$3.3M
Quorum sensing, diversity and skin inflammationR01AI153185 · NIAID · UNIVERSITY OF COLORADO DENVER · PI GALLO, RICHARD L, HORSWILL, ALEXANDER R · 2020 to 2024
$3.2M
Conflict and Cooperation between AMP Species on the skinR01AR076082 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GALLO, RICHARD L, NAKATSUJI, TERUAKI · 2019 to 2023
$2.3M
Staphylococcus hominis bacteriocins protect against skin pathogensR01AI191466 · NIAID · UNIVERSITY OF COLORADO DENVER · PI Richard L Gallo, ALEXANDER R HORSWILL · 2026 to 2026
$767k
NCI NIH HHS P30 CA046592NIAID NIH HHS R01 AI153185NIAID NIH HHS R01 AI191466NIAID NIH HHS R01 AI192662NIAID NIH HHS R37 AI052453NIAID NIH HHS U01 AI152038NIAMS NIH HHS P50 AR080594NIAMS NIH HHS R01 AR076082NIDDK NIH HHS T32 DK007202
6 · The paper itself

Abstract

backgroundSweet syndrome is an inflammatory skin disease characterized by robust neutrophil infiltration into the dermis. The pathogenesis of Sweet syndrome and its distinguishing features compared to other neutrophilic dermatoses, such as pyoderma gangrenosum, remain poorly understood.

objectiveOur aim was to define the cellular and molecular landscape of the skin of patients with Sweet syndrome.

methodsSingle-nucleus and bulk transcriptomics were performed on archival clinical skin samples from patients with Sweet syndrome, patients with pyoderma gangrenosum, and healthy controls. For mechanistic validation, functional experiments were performed with primary human cells. Spatial transcriptomics with single-molecule resolution was used to map cell types to tissue location.

resultsA prominent interferon signature was identified in Sweet syndrome skin that was reduced in tissue samples from patients with pyoderma gangrenosum and healthy controls. This signature was observed in different subsets of cells, including fibroblasts that expressed interferon-induced genes. Functionally, this response was supported by analysis of cultured dermal fibroblasts that were observed to highly express neutrophil chemokines in response to activation by type I interferon. Furthermore, spatial transcriptomics revealed 2 positionally distinct interferon-activated fibroblast subsets: CXCL1-positive fibroblasts near neutrophil infiltrates and CXCL12-positive fibroblasts distal to these infiltrates.

conclusionThis study defines the cellular and molecular landscape of neutrophilic dermatoses and implicates dermal immune-acting fibroblasts in Sweet syndrome pathogenesis through type I interferon recognition and neutrophil recruitment.

Indexed as

FibroblastsInterferonsNeutrophil InfiltrationNeutrophilsSkinSweet SyndromeAdultCells, CulturedFemaleHumansMaleMiddle AgedTranscriptomeInterferonsfibroblastinflammationinterferonneutrophilNeutrophilic dermatosesSweet syndrome

Identifiers

PMID40516577
PMCPMC12678022

What OpenQuestion holds

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Registered trials

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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.