PMID- 31399563
OWN - NLM
STAT- MEDLINE
DCOM- 20191212
LR  - 20210407
IS  - 2041-1723 (Electronic)
IS  - 2041-1723 (Linking)
VI  - 10
IP  - 1
DP  - 2019 Aug 9
TI  - Genetic risk for autoimmunity is associated with distinct changes in the human 
      gut microbiome.
PG  - 3621
LID - 10.1038/s41467-019-11460-x [doi]
LID - 3621
AB  - 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.
FAU - Russell, Jordan T
AU  - Russell JT
AUID- ORCID: 0000-0003-3065-3566
AD  - Department of Microbiology and Cell Science, Institute of Food and Agricultural 
      Sciences University of Florida, Gainesville, 32611-0700, FL, USA.
FAU - Roesch, Luiz F W
AU  - Roesch LFW
AUID- ORCID: 0000-0003-1450-8828
AD  - Biological Sciences, Universidade Federal do Pampa, Sao Gabriel, 97300-000, 
      Brazil.
FAU - Ordberg, Malin
AU  - Ordberg M
AUID- ORCID: 0000-0002-4015-7075
AD  - Crown Princess Victoria's Children's Hospital, Region Ostergotland, Division of 
      Pediatrics, Linkoping University, Linkoping, SE 58185, Sweden.
FAU - Ilonen, Jorma
AU  - Ilonen J
AD  - Immunogenetics Laboratory, Institute of Biomedicine, University of Turku, and 
      Clinical Microbiology, Turku University Hospital, Turku, 20521, Finland.
FAU - Atkinson, Mark A
AU  - Atkinson MA
AUID- ORCID: 0000-0001-8489-4782
AD  - Department of Pathology, University of Florida Diabetes Institute, Gainesville, 
      32610, FL, USA.
AD  - Department of Pediatrics, College of Medicine, University of Florida, 
      Gainesville, 32610, FL, USA.
FAU - Schatz, Desmond A
AU  - Schatz DA
AD  - Department of Pediatrics, College of Medicine, University of Florida, 
      Gainesville, 32610, FL, USA.
FAU - Triplett, Eric W
AU  - Triplett EW
AUID- ORCID: 0000-0002-1845-4866
AD  - Department of Microbiology and Cell Science, Institute of Food and Agricultural 
      Sciences University of Florida, Gainesville, 32611-0700, FL, USA. ewt@ufl.edu.
FAU - Ludvigsson, Johnny
AU  - Ludvigsson J
AD  - Crown Princess Victoria's Children's Hospital, Region Ostergotland, Division of 
      Pediatrics, Linkoping University, Linkoping, SE 58185, Sweden.
LA  - eng
GR  - P01 AI042288/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190809
PL  - England
TA  - Nat Commun
JT  - Nature communications
JID - 101528555
RN  - 0 (Histocompatibility Antigens Class II)
RN  - 0 (RNA, Ribosomal, 16S)
SB  - IM
MH  - Alleles
MH  - Autoimmune Diseases/*genetics
MH  - Autoimmunity/*genetics
MH  - Bacteria/classification/genetics
MH  - Biodiversity
MH  - Celiac Disease/genetics
MH  - Child
MH  - Child, Preschool
MH  - Diabetes Mellitus, Type 1/*immunology
MH  - Feces/microbiology
MH  - Gastrointestinal Microbiome/*immunology
MH  - Genetic Predisposition to Disease/genetics
MH  - Genotype
MH  - Haplotypes
MH  - Histocompatibility Antigens Class II/*genetics
MH  - Humans
MH  - Infant
MH  - RNA, Ribosomal, 16S/genetics
MH  - Risk Factors
MH  - Sweden
PMC - PMC6689114
COIS- The authors declare no competing interests.
EDAT- 2019/08/11 06:00
MHDA- 2019/12/18 06:00
PMCR- 2019/08/09
CRDT- 2019/08/11 06:00
PHST- 2019/02/08 00:00 [received]
PHST- 2019/07/11 00:00 [accepted]
PHST- 2019/08/11 06:00 [entrez]
PHST- 2019/08/11 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
PHST- 2019/08/09 00:00 [pmc-release]
AID - 10.1038/s41467-019-11460-x [pii]
AID - 11460 [pii]
AID - 10.1038/s41467-019-11460-x [doi]
PST - epublish
SO  - Nat Commun. 2019 Aug 9;10(1):3621. doi: 10.1038/s41467-019-11460-x.