Evidence map›Paper›PMID 29182645›Full record

ArticlePloS one2017

HLA and non-HLA genes and familial predisposition to autoimmune diseases in families with a child affected by type 1 diabetes.

Anna Parkkola, Antti-Pekka Laine, Markku Karhunen, Taina Härkönen, Samppa J Ryhänen, Jorma Ilonen, Mikael Knip, Finnish Pediatric Diabetes Register

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. The diabetes pandemic and associated infections: suggestions for clinical microbiology.Reviews in medical microbiology : a journal of the Pathological Society of Great Britain and Ireland · 2019
    Article
  13. Review
  14. 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

8 authors at 2 institutions in 1 country.

Anna ParkkolaScientific Laboratory, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Antti-Pekka LaineImmunogenetics Laboratory, University of Turku, and Turku University Hospital, Turku, Finland.
Markku KarhunenDepartment of Political and Economic Studies, University of Helsinki, Helsinki, Finland.
Taina HärkönenScientific Laboratory, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.
Samppa J RyhänenScientific Laboratory, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.ORCID http://orcid.org/0000-0003-4431-643X
Jorma IlonenImmunogenetics Laboratory, University of Turku, and Turku University Hospital, Turku, Finland.ORCID http://orcid.org/0000-0002-9973-2062
Mikael KnipScientific Laboratory, Children's Hospital, University of Helsinki and Helsinki University Hospital, Helsinki, Finland.ORCID http://orcid.org/0000-0003-0474-0033
Finnish Pediatric Diabetes Register
University of Helsinki · FIUniversity of Turku · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genetic predisposition could be assumed to be causing clustering of autoimmunity in individuals and families. We tested whether HLA and non-HLA loci associate with such clustering of autoimmunity. We included 1,745 children with type 1 diabetes from the Finnish Pediatric Diabetes Register. Data on personal or family history of autoimmune diseases were collected with a structured questionnaire and, for a subset, with a detailed search for celiac disease and autoimmune thyroid disease. Children with multiple autoimmune diseases or with multiple affected first- or second-degree relatives were identified. We analysed type 1 diabetes related HLA class II haplotypes and genotyped 41 single nucleotide polymorphisms (SNPs) outside the HLA region. The HLA-DR4-DQ8 haplotype was associated with having type 1 diabetes only whereas the HLA-DR3-DQ2 haplotype was more common in children with multiple autoimmune diseases. Children with multiple autoimmune diseases showed nominal association with RGS1 (rs2816316), and children coming from an autoimmune family with rs11711054 (CCR3-CCR5). In multivariate analyses, the overall effect of non-HLA SNPs on both phenotypes was evident, associations with RGS1 and CCR3-CCR5 region were confirmed and additional associations were implicated: NRP1, FUT2, and CD69 for children with multiple autoimmune diseases. In conclusion, HLA-DR3-DQ2 haplotype and some non-HLA SNPs contribute to the clustering of autoimmune diseases in children with type 1 diabetes and in their families.

Indexed as

Genetic Predisposition to DiseaseAutoimmune DiseasesChildChild, PreschoolDiabetes Mellitus, Type 1FemaleHaplotypesHLA AntigensHumansMalePolymorphism, Single NucleotideHLA Antigens

Identifiers

PMID29182645
PMCPMC5705143
OpenAlexW2769191240

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.