Genetic risk for autoimmunity is associated with distinct changes in the human gut microbiome.
Alleles
Autoimmune Diseases
/ genetics
Autoimmunity
/ genetics
Bacteria
/ classification
Biodiversity
Celiac Disease
/ genetics
Child
Child, Preschool
Diabetes Mellitus, Type 1
/ immunology
Feces
/ microbiology
Gastrointestinal Microbiome
/ immunology
Genetic Predisposition to Disease
/ genetics
Genotype
Haplotypes
Histocompatibility Antigens Class II
/ genetics
Humans
Infant
RNA, Ribosomal, 16S
/ genetics
Risk Factors
Sweden
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
09 08 2019
09 08 2019
Historique:
received:
08
02
2019
accepted:
11
07
2019
entrez:
11
8
2019
pubmed:
11
8
2019
medline:
18
12
2019
Statut:
epublish
Résumé
Susceptibility to many human autoimmune diseases is under strong genetic control by class II human leukocyte antigen (HLA) allele combinations. These genes remain by far the greatest risk factors in the development of type 1 diabetes and celiac disease. Despite this, little is known about HLA influences on the composition of the human gut microbiome, a potential source of environmental influence on disease. Here, using a general population cohort from the All Babies in Southeast Sweden study, we report that genetic risk for developing type 1 diabetes autoimmunity is associated with distinct changes in the gut microbiome. Both the core microbiome and beta diversity differ with HLA risk group and genotype. In addition, protective HLA haplotypes are associated with bacterial genera Intestinibacter and Romboutsia. Thus, general population cohorts are valuable in identifying potential environmental triggers or protective factors for autoimmune diseases that may otherwise be masked by strong genetic control.
Identifiants
pubmed: 31399563
doi: 10.1038/s41467-019-11460-x
pii: 10.1038/s41467-019-11460-x
pmc: PMC6689114
doi:
Substances chimiques
Histocompatibility Antigens Class II
0
RNA, Ribosomal, 16S
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3621Subventions
Organisme : NIAID NIH HHS
ID : P01 AI042288
Pays : United States
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