Evidence map›Paper›PMID 32743537›Full record

ArticleJournal of translational autoimmunity2020

Aspartic acid

Luis Francisco Valdés-Corona, Susana Hernández-Doño, Tatiana Sofia Rodríguez-Reyna, Rafael García-Silva, Juan Jakez, Monica Escamilla-Tilch, Guadalupe Lima, Luis Llorente, Carlos Pineda, Edmond Yunis and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational autoimmunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
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

11 authors at 4 institutions in 2 countries.

Luis Francisco Valdés-CoronaDepartment of Immunology and Rheumatology, Instituto Nacional de Ciencias Medicas y Nutricion, Salvador Zubiran, Mexico.
Susana Hernández-DoñoImmunogenetics Division, Transplant Department. Instituto Nacional de Ciencias Medicas y Nutricion, Salvador Zubiran, Mexico.
Tatiana Sofia Rodríguez-ReynaDepartment of Immunology and Rheumatology, Instituto Nacional de Ciencias Medicas y Nutricion, Salvador Zubiran, Mexico.
Rafael García-SilvaImmunogenetics Division, Transplant Department. Instituto Nacional de Ciencias Medicas y Nutricion, Salvador Zubiran, Mexico.
Juan JakezDepartment of Immunology and Rheumatology, Instituto Nacional de Ciencias Medicas y Nutricion, Salvador Zubiran, Mexico.
Monica Escamilla-TilchCentro Medico 20 de Noviembre, ISSSTE, Mexico.
Guadalupe LimaDepartment of Immunology and Rheumatology, Instituto Nacional de Ciencias Medicas y Nutricion, Salvador Zubiran, Mexico.
Luis LlorenteDepartment of Immunology and Rheumatology, Instituto Nacional de Ciencias Medicas y Nutricion, Salvador Zubiran, Mexico.
Carlos PinedaInstituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico.
Edmond YunisDepartment of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, USA.
Julio GranadosImmunogenetics Division, Transplant Department. Instituto Nacional de Ciencias Medicas y Nutricion, Salvador Zubiran, Mexico.
Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán · MXDana-Farber Cancer Institute · USInstitute for Social Security and Services for State Workers · MXInstituto Nacional de Rehabilitación · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAutoimmune thyroid disease (AITD) is the most common autoimmune disorder worldwide. Remarkably, it is commonly accompanied by other autoimmune diseases, such as rheumatoid arthritis (RA). The immunopathogenic mechanisms behind the coexistence of these disorders are still not completely understood. Immunogenetics influences the physiopathology of these diseases since ethnicity plays an essential role in the inheritance of susceptibility markers.

methodsHigh-resolution HLA class II typing was performed using a sequence-based method.

resultsThe allele frequency of HLA-DRB1∗04:04 and -DRB1∗03:01 were significantly increased in patients with AITD and RA compared to healthy individuals, pC ​= ​0.021, OR ​= ​2.4, 95%CI ​= ​1.19-4.75 and pC ​= ​0.009, OR ​= ​3.4, 95%CI ​= ​1.42-7.93, respectively. Remarkably, these patients have a combined risk given by susceptibility HLA-DRB1 alleles that contain the shared epitope, pC ​= ​0.03, OR ​= ​1.7, IC95% ​= ​1.07-2.76, and a lack of protective alleles carrying aspartic acid DISCUSSION: The results suggest that patients with AITD and RA have an immunogenetic mechanism that combines the susceptibility alleles associated with both diseases. Importantly, it seems to be linked mainly to the lack of protective alleles with aspartic acid in the position 70, along with the presence of susceptibility alleles that have the sequences QRRAA, QKRAA, and RRRAA at positions 70-74.

conclusionPatients with AITD and RA have a characteristic immunogenetic signature, which could be useful for determining multiple autoimmunities and assessing their relatives' risk of developing it.

Indexed as

Autoimmune thyroid diseaseGraves’ diseaseHashimoto’s diseaseHLA-DRB1Multiple autoimmunitiesRheumatoid arthritisShared epitope

Identifiers

PMID32743537
PMCPMC7388401
OpenAlexW3025541431

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.