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GWAS Study

GWAS for autoimmune Addison's disease identifies multiple risk loci and highlights AIRE in disease susceptibility.

Eriksson D, Røyrvik EC, Aranda-Guillén M et al.

33574239 PubMed ID
GWAS Study Type
5320 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

ED
Eriksson D
RE
Røyrvik EC
AM
Aranda-Guillén M
BA
Berger AH
LN
Landegren N
AH
Artaza H
Hallgren Å
GM
Grytaas MA
SS
Ström S
BE
Bratland E
BI
Botusan IR
OB
Oftedal BE
BL
Breivik L
VM
Vaudel M
Helgeland Ø
FA
Falorni A
JA
Jørgensen AP
HA
Hulting AL
SJ
Svartberg J
EO
Ekwall O
FK
Fougner KJ
WJ
Wahlberg J
NB
Nedrebø BG
DP
Dahlqvist P
KP
Knappskog PM
WA
Wolff ASB
BS
Bensing S
JS
Johansson S
KO
Kämpe O
HE
Husebye ES
Chapter II

Abstract

Summary of the research findings

Autoimmune Addison's disease (AAD) is characterized by the autoimmune destruction of the adrenal cortex. Low prevalence and complex inheritance have long hindered successful genetic studies. We here report the first genome-wide association study on AAD, which identifies nine independent risk loci (P < 5 × 10-8). In addition to loci implicated in lymphocyte function and development shared with other autoimmune diseases such as HLA, BACH2, PTPN22 and CTLA4, we associate two protein-coding alterations in Autoimmune Regulator (AIRE) with AAD. The strongest, p.R471C (rs74203920, OR = 3.4 (2.7-4.3), P = 9.0 × 10-25) introduces an additional cysteine residue in the zinc-finger motif of the second PHD domain of the AIRE protein. This unbiased elucidation of the genetic contribution to development of AAD points to the importance of central immunological tolerance, and explains 35-41% of heritability (h2).

1,223 European ancestry cases, 4,097 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

5320
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
Norway, Sweden
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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