Evidence map›Paper›PMID 26343334›Full record

ReviewJournal of autoimmunity2015

The genetics of human autoimmune disease: A perspective on progress in the field and future directions.

Michael F Seldin

Abstract readReview
In one paragraph

Review in Journal of autoimmunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.4field-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

38 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. [Exploring the research on the molecular mechanisms of autoimmune liver diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Review
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  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Pathogenesis of Autoimmune Hepatitis-Cellular and Molecular Mechanisms.International journal of molecular sciences · 2021
    Review
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

1 author at 1 institution in 1 country.

Michael F SeldinDepartment of Biochemistry and Molecular Medicine, University of California, Davis, Tupper Hall Room 4453, Davis, CA 95616, USA; Division of Rheumatology and Allergy, Department of Medicine, University of California, Davis, Tupper Hall Room 4453, Davis, CA 95616, USA. Electronic address: mfseldin@ucdavis.edu.
University of California, Davis · US

Funding

IDENTIFICATION OF COMMON AND UNCOMMON GENE VARIANTS IN PBCR01DK091823 · NIDDK · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GERSHWIN, MERRILL E, KINGSMORE, STEPHEN FRANCIS · 2011 to 2014
$2.4M
NIDDK NIH HHS R01 DK091823NIDDK NIH HHS R01DK091823
6 · The paper itself

Abstract

Progress in defining the genetics of autoimmune disease has been dramatically enhanced by large scale genetic studies. Genome-wide approaches, examining hundreds or for some diseases thousands of cases and controls, have been implemented using high throughput genotyping and appropriate algorithms to provide a wealth of data over the last decade. These studies have identified hundreds of non-HLA loci as well as further defining HLA variations that predispose to different autoimmune diseases. These studies to identify genetic risk loci are also complemented by progress in gene expression studies including definition of expression quantitative trait loci (eQTL), various alterations in chromatin structure including histone marks, DNase I sensitivity, repressed chromatin regions as well as transcript factor binding sites. Integration of this information can partially explain why particular variations can alter proclivity to autoimmune phenotypes. Despite our incomplete knowledge base with only partial definition of hereditary factors and possible functional connections, this progress has and will continue to facilitate a better understanding of critical pathways and critical changes in immunoregulation. Advances in defining and understanding functional variants potentially can lead to both novel therapeutics and personalized medicine in which therapeutic approaches are chosen based on particular molecular phenotypes and genomic alterations.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseAnimalsAutoimmune DiseasesEpigenesis, GeneticEpistasis, GeneticGene Expression RegulationGenetic LociGenetic VariationGenome-Wide Association StudyGenomicsHumansMajor Histocompatibility ComplexPhenotypeAutoimmune diseasesFunctional variantsGeneticsHLAImmunoregulationSusceptibility loci

Identifiers

PMID26343334
PMCPMC4628839
OpenAlexW1550706719

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.