Evidence map›Paper›PMID 39276210›Full record

ArticleImmunogenetics2024

Potential contribution of gut microbiota in the development of autoantibodies in T1D children carrying HLA-DRB1/DQB1 risk alleles: an experimental and in silico analysis.

Ata Shirizadeh, Zahra Razavi, Vahid Saeedi, Mahdi Behzad, Javad Faradmal, Ghasem Solgi

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Article in Immunogenetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

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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

2 citing papers in PubMed.

  1. Observational
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4 · The record

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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

6 authors.

Ata ShirizadehImmunology Department, Medical School, Hamadan University of Medical Sciences, Shahid Fahmideh Blvd, Opposite to Lona Park, P.O. Box: 6517838736, Hamadan, Iran.
Zahra RazaviPediatrics Department, Medical School, Hamadan University of Medical Sciences, Hamadan, Iran.
Vahid SaeediPediatric Endocrinology and Metabolism Department, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Mahdi BehzadImmunology Department, Medical School, Hamadan University of Medical Sciences, Shahid Fahmideh Blvd, Opposite to Lona Park, P.O. Box: 6517838736, Hamadan, Iran.
Javad FaradmalBiostatistics Department, Health School, Hamadan University of Medical Sciences, Hamadan, Iran.
Ghasem SolgiImmunology Department, Medical School, Hamadan University of Medical Sciences, Shahid Fahmideh Blvd, Opposite to Lona Park, P.O. Box: 6517838736, Hamadan, Iran. gh.solgi@umsha.ac.ir.ORCID 0000-0001-8929-5658

Funding

Vice Chancellor for Research and Technology, Hamadan University of Medical Sciences 140110279119
6 · The paper itself

Abstract

This study aimed to investigate the prevalence of insulin autoantibody (IAA), glutamic acid decarboxylase antibody (GADA), and insulinoma-associated antigen-2 antibody (IA-2A) in type 1 diabetes (T1D) children based on the presence of predisposing HLA-II alleles. Additionally, to assess the sequence homology between autoantigens of islet cells and selected proteins derived from gut bacteria in terms of their binding capacities to HLA risk alleles, HLA-DRB1/DQB1 alleles were determined by PCR-SSOP in 111 T1D children (probands) along with 222 parents and 133 siblings. Autoantibodies were measured by ELISA, and in silico analysis was run as follows: protein extraction, homology and epitope prediction, peptide alignment, and HLA-peptide docking. Higher significant frequencies of DRB1*03:01, DQB1*02:01, and DQB1*03:02 alleles and DRB1*03:01 ~ DQB1*02:01 haplotype and lower frequencies of DRB1*11:01, DRB1*14:01, and DQB1*03:01 alleles were found in probands compared to parents and siblings. DRB1*11:01 ~ DQB1*03:01, DRB1*14:01 ~ DQB1*05:03, and DRB1*15:01-DQB1*06:02 haplotypes were significantly less frequent in the probands compared to parents. Out of 111 probands, 21 were seronegative, 90 tested positive for one autoantibody, and 15 showed the concurrent presence of three autoantibodies. Logistic regression analysis revealed that DRB1*04 ~ DQB1*03:02 haplotype was associated with the induction of GADA and IA-2A, while DRB1*11:01 ~ DQB1*03:01 was associated with seronegativity. Epitopes derived from GAD and gut bacteria showed strong binding capacities to HLA risk alleles. Due to the sequence similarities between gut bacteria-derived proteins and islet cell autoantigens and their potential for binding to HLA risk alleles, dysbiosis of gut microbiota can be considered another risk factor for the development of T1D, especially in genetically susceptible individuals.

Indexed as

AllelesAutoantibodiesDiabetes Mellitus, Type 1Gastrointestinal MicrobiomeGenetic Predisposition to DiseaseHLA-DQ beta-ChainsHLA-DRB1 ChainsAdolescentChildChild, PreschoolComputer SimulationFemaleGlutamate DecarboxylaseHaplotypesHumansMaleAutoantibodiesGlutamate DecarboxylaseHLA-DQB1 antigenHLA-DQ beta-ChainsHLA-DRB1 ChainsReceptor-Like Protein Tyrosine Phosphatases, Class 8AutoantibodyHLA-DRB1/DQB1In silicoMicrobiotaT1D

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Registered trials

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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.