Evidence map›Paper›PMID 37141355›Full record

ReviewScience (New York, N.Y.)2023

Common genetic factors among autoimmune diseases.

Adil Harroud, David A Hafler

Abstract readReview
In one paragraph

Review in Science (New York, N.Y.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
–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

58 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Genome-scale perturbation signatures from primary human CD4bioRxiv : the preprint server for biology · 2026
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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.

Adil HarroudDepartment of Neurology and Neurosurgery, McGill University, Montréal, Quebec, Canada.ORCID 0000-0003-2616-7274
David A HaflerDepartment of Neurology, Yale School of Medicine, New Haven, CT, USA.ORCID 0000-0003-4664-535X

Funding

Yale SPORE in Skin CancerP50CA121974 · NCI · YALE UNIVERSITY · PI DAVID F STERN · 2006 to 2026
$43.9M
Transgenic / Knock-out mouse coreP01AI073748 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BEHAR, SAMUEL M · 2008 to 2019
$17.1M
The function of T Bet in EAEP01NS038037 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 2000 to 2010
$12.8M
A Catalog of Cell Types and Genomic Elements in Tissues, Organoids and DiseaseUM1HG009390 · NHGRI · BROAD INSTITUTE, INC. · PI BERNSTEIN, BRADLEY EVAN · 2017 to 2021
$11.0M
(8) Mechanisms of autoimmune endocrine diseases in patients receiving checkpoint inhibitorsR01CA227473 · NCI · YALE UNIVERSITY · PI HEROLD, KEVAN C, KLUGER, HARRIET M. · 2018 to 2022
$3.2M
Genomics of NFκB-mediated gene regulation in multiple sclerosisR01AI122220 · NIAID · YALE UNIVERSITY · PI COTSAPAS, CHRIS · 2016 to 2019
$2.9M
NCI NIH HHS P50 CA121974NCI NIH HHS R01 CA227473NHGRI NIH HHS UM1 HG009390NIAID NIH HHS P01 AI073748NIAID NIH HHS R01 AI122220NINDS NIH HHS P01 NS038037
6 · The paper itself

Abstract

Autoimmune diseases display a high degree of comorbidity within individuals and families, suggesting shared risk factors. Over the past 15 years, genome-wide association studies have established the polygenic basis of these common conditions and revealed widespread sharing of genetic effects, indicative of a shared immunopathology. Despite ongoing challenges in determining the precise genes and molecular consequences of these risk variants, functional experiments and integration with multimodal genomic data are providing valuable insights into key immune cells and pathways driving these diseases, with potential therapeutic implications. Moreover, genetic studies of ancient populations are shedding light on the contribution of pathogen-driven selection pressures to the increased prevalence of autoimmune disease. This Review summarizes the current understanding of autoimmune disease genetics, including shared effects, mechanisms, and evolutionary origins.

Indexed as

Autoimmune DiseasesGenetic Predisposition to DiseaseGenomeGenome-Wide Association StudyHumansRisk Factors

Identifiers

PMID37141355
PMCPMC13069990

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.