Menu
GWAS Study

Genome-wide meta-analysis in alopecia areata resolves HLA associations and reveals two new susceptibility loci.

Betz RC, Petukhova L, Ripke S et al.

25608926 PubMed ID
GWAS Study Type
10585 Participants
Scroll to explore
Chapter I

Publication Details

Comprehensive information about this research publication

Authors

BR
Betz RC
PL
Petukhova L
RS
Ripke S
HH
Huang H
MA
Menelaou A
RS
Redler S
BT
Becker T
HS
Heilmann S
YT
Yamany T
DM
Duvic M
HM
Hordinsky M
ND
Norris D
PV
Price VH
MJ
Mackay-Wiggan J
DJ
de Jong A
DG
DeStefano GM
MS
Moebus S
BM
Böhm M
BU
Blume-Peytavi U
WH
Wolff H
LG
Lutz G
KR
Kruse R
BL
Bian L
AC
Amos CI
LA
Lee A
GP
Gregersen PK
BB
Blaumeiser B
AD
Altshuler D
CR
Clynes R
DB
de Bakker PIW
NM
Nöthen MM
DM
Daly MJ
CA
Christiano AM
Chapter II

Abstract

Summary of the research findings

Alopecia areata (AA) is a prevalent autoimmune disease with 10 known susceptibility loci. Here we perform the first meta-analysis of research on AA by combining data from two genome-wide association studies (GWAS), and replication with supplemented ImmunoChip data for a total of 3,253 cases and 7,543 controls. The strongest region of association is the major histocompatibility complex, where we fine-map four independent effects, all implicating human leukocyte antigen-DR as a key aetiologic driver. Outside the major histocompatibility complex, we identify two novel loci that exceed the threshold of statistical significance, containing ACOXL/BCL2L11(BIM) (2q13); GARP (LRRC32) (11q13.5), as well as a third nominally significant region SH2B3(LNK)/ATXN2 (12q24.12). Candidate susceptibility gene expression analysis in these regions demonstrates expression in relevant immune cells and the hair follicle. We integrate our results with data from seven other autoimmune diseases and provide insight into the alignment of AA within these disorders. Our findings uncover new molecular pathways disrupted in AA, including autophagy/apoptosis, transforming growth factor beta/Tregs and JAK kinase signalling, and support the causal role of aberrant immune processes in AA.

2,332 European ancestry cases and 5,233 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

10585
Total Participants
GWAS
Study Type
Yes
Replicated
764 European ancestry cases and 2,256 European ancestry controls
Replication Participants
European
Ancestry
U.S., Belgium, Germany
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

Important Disclaimer: This review has been performed semi-automatically and is provided for informational purposes only. While we strive for accuracy, this analysis may contain errors, omissions, or misinterpretations of the original research. DNA Genics disclaims all liability for any inaccuracies, errors, or consequences arising from the use of this information. Users should independently verify all information and consult original research publications before making any decisions based on this content. This analysis is not intended as a substitute for professional scientific review or medical advice.

Analysis In Progress

Our analysis of this publication is currently being prepared. Please check back soon for comprehensive insights into the health and genetic findings discussed in this research.