Evidence map›Paper›PMID 27764715›Full record

ReviewCurrent opinion in immunology2016

Understanding mechanisms of autoimmunity through translational research in vitiligo.

James P Strassner, John E Harris

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current opinion in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 68 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

James P StrassnerDepartment of Medicine, Division of Dermatology, University of Massachusetts Medical School, 364 Plantation St., LRB 225, Worcester, MA 01605, USA.
John E HarrisDepartment of Medicine, Division of Dermatology, University of Massachusetts Medical School, 364 Plantation St., LRB 225, Worcester, MA 01605, USA. Electronic address: john.harris@umassmed.edu.
University of Massachusetts Chan Medical School · US

Funding

Treg Migration and Function During Autoimmunity within Peripheral TissueR01AR069114 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HARRIS, JOHN E · 2015 to 2020
$2.2M
Targeting IFN gamma and chemokines to treat vitiligo in a humanized mouse modelK08AR061437 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HARRIS, JOHN E · 2011 to 2015
$619k
NIAMS NIH HHS K08 AR061437NIAMS NIH HHS R01 AR069114
6 · The paper itself

Abstract

Vitiligo is an autoimmune disease of the skin that leads to life-altering depigmentation and remains difficult to treat. However, clinical observations and translational studies over 30-40 years have led to the development of an insightful working model of disease pathogenesis: Genetic risk spanning both immune and melanocyte functions is pushed over a threshold by known and suspected environmental factors to initiate autoimmune T cell-mediated killing of melanocytes. While under cellular stress, melanocytes appear to signal innate immunity to activate T cells. Once the autoimmune T cell response is established, the IFN-γ-STAT1-CXCL10 signaling axis becomes the primary inflammatory pathway driving both progression and maintenance of vitiligo. This pathway is a tempting target for both existing and developing pharmaceuticals, but further detailing how melanocytes signal their own demise may also lead to new therapeutic targets. Research in vitiligo may be the future key to understand the pathogenesis of organ-specific autoimmunity, as vitiligo is common, reversible, progresses over the life of the individual, has been relatively well-defined, and is quite easy to study using translational and clinical approaches. What is revealed in these studies can lead to innovative treatments and also help elucidate the principles that underlie similar organ-specific autoimmune diseases, especially in cases where the target organ is less accessible.

Indexed as

AutoimmunityAnimalsChemokine CXCL10Gene-Environment InteractionHumansImmunity, InnateInterferon-gammaMelanocytesRiskSignal TransductionSkinSTAT1 Transcription FactorT-LymphocytesTranslational Research, BiomedicalVitiligoChemokine CXCL10Interferon-gammaSTAT1 Transcription Factor

Identifiers

PMID27764715
PMCPMC5292941
OpenAlexW2536042267

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.