Evidence map›Paper›PMID 30515176›Full record

Trial reportFrontiers in immunology2018

Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis.

Liisi Raam, Epp Kaleviste, Marina Šunina, Helen Vaher, Mario Saare, Ele Prans, Maire Pihlap, Kristi Abram, Maire Karelson, Pärt Peterson and 3 more

Open access · goldAbstract readClinical Trial
In one paragraph

Trial report in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  13. Increased Serum Levels of IFN-Oxidative medicine and cellular longevity · 2020
    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

13 authors at 2 institutions in 1 country.

Liisi RaamDepartment of Dermatology, University of Tartu, Tartu, Estonia.
Epp KalevisteInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Marina ŠuninaInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Helen VaherInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Mario SaareInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Ele PransInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Maire PihlapInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Kristi AbramDepartment of Dermatology, University of Tartu, Tartu, Estonia.
Maire KarelsonDepartment of Dermatology, University of Tartu, Tartu, Estonia.
Pärt PetersonInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Ana RebaneInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Kai KisandInstitute of Biomedicine and Translational Medicine, University of Tartu, Tartu, Estonia.
Külli KingoDepartment of Dermatology, University of Tartu, Tartu, Estonia.
University of Tartu · EETartu University Hospital · EE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vitiligo is a chronic multifactorial depigmentation disorder characterized by the destruction and functional loss of melanocytes. Although a direct cytotoxic T cell attack is thought to be responsible for melanocyte damage, the events leading to the loss of self-tolerance toward melanocytic antigens are not understood. This research aimed to identify novel cellular and molecular factors that participate in vitiligo pathogenesis through the application of gene expression and immunofluorescence analysis of skin biopsy samples along with immunophenotyping of circulating cells. Our study provides insights into the mechanisms involved in melanocyte destruction. The upregulation of stress-ligand MICA/MICB, recognized by activating receptors on innate and innate-like T cells, imply involvement of lymphoid stress surveillance responses in vitiligo lesions. A simultaneous increase in the expression of transcription factor

Indexed as

Immunity, HumoralAdultAutophagyB-LymphocytesFemaleHistocompatibility Antigens Class IHumansKeratinocytesMaleMelanocytesMiddle AgedStress, PhysiologicalT-Box Domain ProteinsT-Lymphocytes, Helper-InducerVitiligoEOMES protein, humanHistocompatibility Antigens Class IMHC class I-related chain AMICB antigenT-Box Domain ProteinsautophagyB cellsEOMESinterferonsLC3MICA/MICBvitiligoWIPI1

Identifiers

PMID30515176
PMCPMC6255962
OpenAlexW2900630656

What OpenQuestion holds

Textmetadata
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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.