Evidence map›Paper›PMID 18178059›Full record

ReviewJournal of autoimmunity

The HLA gene complex in thyroid autoimmunity: from epidemiology to etiology.

Eric M Jacobson, Amanda Huber, Yaron Tomer

Open access · greenAbstract readReview
In one paragraph

Review in Journal of autoimmunity. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 98 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
98citing papers in PubMed, 2 pooled it
14.5field-weighted citation impact, top 1% 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

98 citing papers in PubMed, 2 syntheses or guidelines pooled it, 245 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. [Role of HLA genetic variants in autoimmune diseases].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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  16. HLA Polymorphisms and Clinical Manifestations in IgA Vasculitis.International journal of molecular sciences · 2024
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38 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Eric M JacobsonDivision of Endocrinology, Cincinnati VA Medical Center, Cincinnati, OH, USA.
Amanda Huber
Yaron Tomer
Cincinnati VA Medical Center · USUniversity of Cincinnati Medical Center · US

Funding

Mapping Autoimmune Diabetes and Thyroiditis GenesR01DK067555 · NIDDK · UNIVERSITY OF CINCINNATI · PI MIHAELA STEFAN LIFSHITZ, YARON TOMER · 2005 to 2026
$5.8M
Thyroid Derived Peptide Presentation by HLA-DR in ThyroiditisR01DK073681 · NIDDK · UNIVERSITY OF CINCINNATI · PI TOMER, YARON · 2006 to 2022
$5.0M
Identifying Genes Linked to Autoimmune Thyroid DiseasesR01DK061659 · NIDDK · UNIVERSITY OF CINCINNATI · PI TOMER, YARON · 2002 to 2017
$4.1M
Obesity and Surgical OutcomesR01DK073671 · NIDDK · CHILDREN'S HOSP OF PHILADELPHIA · PI SILBER, JEFFREY H · 2006 to 2010
$3.1M
NIDDK NIH HHS DK067555NIDDK NIH HHS DK073671NIDDK NIH HHS DK61659NIDDK NIH HHS R01 DK061659NIDDK NIH HHS R01 DK067555NIDDK NIH HHS R01 DK073681
6 · The paper itself

Abstract

The autoimmune thyroid diseases (AITD) comprise a cadre of complex diseases whose underlying pathoetiology stems from a genetic-environmental interaction, between susceptibility genes (e.g. CTLA-4, HLA-DR, thyroglobulin) and environmental triggers (e.g. dietary iodine), that orchestrates the initiation of an autoimmune response to thyroid antigens, leading to the onset of disease. Abundant epidemiological data, including family and twin studies, point to a strong genetic influence on the development of AITD. Several AITD susceptibility genes have been identified, with HLA genes, in particular, appearing to be of major importance. Early studies showed association of HLA-DR3 with Graves' disease (GD) in Caucasians. More recently, the importance of an amino acid substitution at position 74 of the DR beta 1 chain of HLA-DR3 (DRb1-Arg74), in susceptibility to Graves' disease, has been shown. Furthermore, there is increasing evidence for a genetic interaction between thyroglobulin variants and DRb1-Arg74 in conferring risk for GD. Mechanistically, the presence of an arginine at position 74 elicits a significant structural change in the peptide binding pocket of HLA-DR, potentially affecting the binding of pathogenic thyroidal peptides. Future therapeutic interventions may attempt to exploit this new bolus of knowledge by endeavoring to block or modulate pathogenic peptide presentation by HLA-DR.

Indexed as

Genes, MHC Class IGenes, MHC Class IIAutoantibodiesAutoimmunityGenetic Predisposition to DiseaseGraves DiseaseHashimoto DiseaseHLA-DR AntigensHumansPolymorphism, GeneticThyroglobulinThyroid GlandAutoantibodiesHLA-DR AntigensThyroglobulin

Identifiers

PMID18178059
PMCPMC2244911
OpenAlexW1969255934

What OpenQuestion holds

Textmetadata
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.