Evidence map›Paper›PMID 41918735›Full record

ReviewFrontiers in immunology2026

The role of JAK3 and TEC family kinases in vitiligo pathogenesis.

Thierry Passeron, Julien Seneschal, Mauro Picardo, Leihong Xiang, Atsushi Tanemura, Aaron Winkler, Jean-Baptiste Telliez, Roni Adiri

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2026. 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

8 authors.

Thierry PasseronUniversity Côte d'Azur, Centre Hospitalier Universitaire Nice, Department of Dermatology, Nice, France.
Julien SeneschalCentre Hospitalier Universitaire (CHU) de Bordeaux, Department of Dermatology and Pediatric Dermatology, National Reference Center for Rare Skin Diseases, Hôpital Saint-André, UMR 5164, Bordeaux, France.
Mauro PicardoIstituto Dermopatico Immacolata, Scientific Hospitalization and Treatment Institute (IRCCS), Rome, Italy.
Leihong XiangDepartment of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.
Atsushi TanemuraDepartment of Dermatology Integrated Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
Aaron WinklerInflammation and Immunology Research Unit, Pfizer Inc., Cambridge, MA, United States.
Jean-Baptiste TelliezInflammation and Immunology Research Unit, Pfizer Inc., Cambridge, MA, United States.
Roni AdiriPfizer Pharmaceutical Israel LTD, Herzliya Pituach, Israel.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vitiligo is an autoimmune disease characterized by the loss of skin pigmentation due to the loss of melanocytes. The pathogenesis of vitiligo is complex, involving multiple genetic factors, environmental triggers, oxidative stress, and autoimmunity against melanocytes. Stressed melanocytes release damage-associated molecular patterns, which trigger increased activation of antigen presenting cells, leading to maturation and activation of CD8

Indexed as

Janus Kinase 3Protein-Tyrosine KinasesVitiligoAnimalsCytokinesHumansMelanocytesSignal TransductionSTAT Transcription FactorsCytokinesJAK3 protein, humanJanus Kinase 3Protein-Tyrosine KinasesSTAT Transcription FactorsTec protein-tyrosine kinaseautoimmune disordercytokinedisease pathogenesisJAK3 (Janus kinase 3)JAK-STAT signaling pathwaytargeted therapyTEC family kinasesvitiligo

Identifiers

PMID41918735
PMCPMC13033657

What OpenQuestion holds

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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.