Evidence map›Paper›PMID 40286789›Full record

ArticleCell genomics2025

Effects of parental autoimmune diseases on type 1 diabetes in offspring can be partially explained by HLA and non-HLA polymorphisms.

Feiyi Wang, Aoxing Liu, Zhiyu Yang, Pekka Vartiainen, Sakari Jukarainen, Satu Koskela, Richard Oram, Lowri Allen, Jarmo Ritari, Jukka Partanen and 4 more

Abstract read
In one paragraph

Article in Cell genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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

4 citing papers in PubMed.

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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

14 authors.

Feiyi WangInstitute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Helsinki, Finland; Centre for Population Health Sciences, Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, Scotland.
Aoxing LiuInstitute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Helsinki, Finland; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA; Center for Genomic Medicine, Massachusetts General Hospital, Boston, MA, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA, USA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge, MA, USA.
Zhiyu YangInstitute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Helsinki, Finland.
Pekka VartiainenInstitute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Helsinki, Finland.
Sakari JukarainenInstitute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Helsinki, Finland.
Satu KoskelaFinnish Red Cross Blood Service, Helsinki, Finland.
Richard OramUniversity of Exeter, Exeter, UK.
Lowri AllenCardiff University and University Hospital of Wales, Cardiff, UK.
Jarmo RitariFinnish Red Cross Blood Service, Helsinki, Finland.
Jukka PartanenFinnish Red Cross Blood Service, Helsinki, Finland.
FinnGen
Markus PerolaFinnish Institute for Health and Welfare (THL), Helsinki, Finland.
Tiinamaija TuomiInstitute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Helsinki, Finland; Abdominal Center, Endocrinology, Helsinki University Hospital, Helsinki, Finland; Folkhälsan Research Center, Helsinki, Finland; Lund University Diabetes Center, Malmö, Sweden. Electronic address: tiinamaija.tuomi@hus.fi.
Andrea GannaInstitute for Molecular Medicine Finland (FIMM), Helsinki Institute of Life Science (HiLIFE), University of Helsinki, Helsinki, Finland; Analytic and Translational Genetics Unit, Massachusetts General Hospital, Boston, MA, USA; Program in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, MA, USA; Stanley Center for Psychiatric Research, Broad Institute of Harvard and MIT, Cambridge, MA, USA. Electronic address: andrea.ganna@helsinki.fi.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) and other autoimmune diseases (AIDs) often co-occur in families. Leveraging data from 58,284 family trios in Finnish nationwide registers (FinRegistry), we identified that, of 50 parental AIDs examined, 15 were associated with an increased T1D risk in offspring. These identified epidemiological associations were further assessed in 470,000 genotyped Finns from the FinnGen study through comprehensive genetic analyses, partitioned into human leukocyte antigen (HLA) and non-HLA variations. Using FinnGen's 12,563 trios, a within-family polygenic transmission analysis demonstrated that the aggregation of many parental AIDs with offspring T1D can be partially explained by HLA and non-HLA polymorphisms in a disease-dependent manner. We therefore proposed a parental polygenic score (PGS), incorporating both HLA and non-HLA polymorphisms, to characterize the cumulative risk pattern of T1D in offspring. This raises an intriguing possibility of using parental PGS, in conjunction with clinical diagnoses, to inform individuals about T1D risk in their offspring.

Indexed as

Autoimmune DiseasesDiabetes Mellitus, Type 1HLA AntigensPolymorphism, GeneticAdultChildFemaleFinlandGenetic Predisposition to DiseaseGenotypeHumansMaleMultifactorial InheritanceParentsPolymorphism, Single NucleotideRegistriesHLA Antigensautoimmune diseaseceliac diseasefamily historygenetic correlationHLAmajor histocompatibility complexmulti-trait PRSpolygenic risk scorepolygenic transmission disequilibrium testrheumatoid arthritistype 1 diabetes

Identifiers

PMID40286789
PMCPMC12230240

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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.