Evidence map›Paper›PMID 35979360›Full record

ReviewFrontiers in immunology2022

Genetic basis of defects in immune tolerance underlying the development of autoimmunity.

Anne M Hocking, Jane H Buckner

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  11. Article
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  13. Special Issue "Advances in Molecular Research on Autoimmune Diseases".International journal of molecular sciences · 2024
    Article
  14. Article
  15. Climate Stressors and Physiological Dysregulations: Mechanistic Connections to Pathologies.International journal of environmental research and public health · 2023
    Review
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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.

Anne M HockingCenter for Translational Immunology, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.
Jane H BucknerCenter for Translational Immunology, Benaroya Research Institute at Virginia Mason, Seattle, WA, United States.
Virginia Mason Medical Center · US

Funding

Mechanisms of IL-6 mediated T cell pathogenesis in autoimmunityR01AI132774 · NIAID · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2017 to 2020
$6.4M
Defining the functional impact of T1D genes in mouse and man: a unified strategyDP3DK097672 · NIDDK · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2012 to 2013
$4.4M
Exploring novel disease mechanisms in RA linked to HLA class II riskR21AR073508 · NIAMS · BENAROYA RESEARCH INST AT VIRGINIA MASON · PI BUCKNER, JANE HOYT · 2018 to 2019
$401k
NIAID NIH HHS R01 AI132774NIAMS NIH HHS R21 AR073508NIDDK NIH HHS DP3 DK097672
6 · The paper itself

Abstract

Genetic variants associated with susceptibility to autoimmune disease have provided important insight into the mechanisms responsible for the loss of immune tolerance and the subsequent development of autoantibodies, tissue damage, and onset of clinical disease. Here, we review how genetic variants shared across multiple autoimmune diseases have contributed to our understanding of global tolerance failure, focusing on variants in the human leukocyte antigen region, PTPN2 and PTPN22, and their role in antigen presentation and T and B cell homeostasis. Variants unique to a specific autoimmune disease such as those in PADI2 and PADI4 that are associated with rheumatoid arthritis are also discussed, addressing their role in disease-specific immunopathology. Current research continues to focus on determining the functional consequences of autoimmune disease-associated variants but has recently expanded to variants in the non-coding regions of the genome using novel approaches to investigate the impact of these variants on mechanisms regulating gene expression. Lastly, studying genetic risk variants in the setting of autoimmunity has clinical implications, helping predict who will develop autoimmune disease and also identifying potential therapeutic targets.

Indexed as

Arthritis, RheumatoidAutoimmune DiseasesAutoantibodiesAutoimmunityHumansImmune ToleranceProtein Tyrosine Phosphatase, Non-Receptor Type 22AutoantibodiesProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humanautoimmunitygenetic variantsHLAimmune toleranceINS-VNTRPADIPTPN2PTPN22

Identifiers

PMID35979360
PMCPMC9376219
OpenAlexW4289130226

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.