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GWAS Study

Early-onset autoimmune vitiligo associated with an enhancer variant haplotype that upregulates class II HLA expression.

Jin Y, Roberts GHL, Ferrara TM et al.

30674883 PubMed ID
GWAS Study Type
22327 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

JY
Jin Y
RG
Roberts GHL
FT
Ferrara TM
BS
Ben S
VG
van Geel N
WA
Wolkerstorfer A
EK
Ezzedine K
SJ
Siebert J
NC
Neff CP
PB
Palmer BE
SS
Santorico SA
SR
Spritz RA
Chapter II

Abstract

Summary of the research findings

Vitiligo is an autoimmune disease in which melanocyte destruction causes skin depigmentation, with 49 loci known from previous GWAS. Aiming to define vitiligo subtypes, we discovered that age-of-onset is bimodal; one-third of cases have early onset (mean 10.3 years) and two-thirds later onset (mean 34.0 years). In the early-onset subgroup we found novel association with MHC class II region indel rs145954018, and independent association with the principal MHC class II locus from previous GWAS, represented by rs9271597; greatest association was with rs145954018del-rs9271597A haplotype (P = 2.40 × 10-86, OR = 8.10). Both rs145954018 and rs9271597 are located within lymphoid-specific enhancers, and the rs145954018del-rs9271597A haplotype is specifically associated with increased expression of HLA-DQB1 mRNA and HLA-DQ protein by monocytes and dendritic cells. Thus, for vitiligo, MHC regulatory variation confers extreme risk, more important than HLA coding variation. MHC regulatory variation may represent a significant component of genetic risk for other autoimmune diseases.

1,467 European ancestry cases, 19,156 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

22327
Total Participants
GWAS
Study Type
Yes
Replicated
977 European ancestry cases, 727 European ancestry controls
Replication Participants
European
Ancestry
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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