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GWAS Study

Shared genetic study gives insights into the shared and distinct pathogenic immunity components of IgA nephropathy and SLE.

Zhang YM, Zhou XJ, Wang YN et al.

34076728 PubMed ID
GWAS Study Type
2079 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

ZY
Zhang YM
ZX
Zhou XJ
WY
Wang YN
LX
Liu XZ
WY
Wang YF
LY
Lau YL
YW
Yang WL
ZH
Zhang H
Chapter II

Abstract

Summary of the research findings

An autoimmune component has been suggested to play a role in pathogenesis of IgA nephropathy (IgAN). And genetic studies have reported the shared susceptibility loci between IgAN and the prototype autoimmune disease systemic lupus erythematosus (SLE). This study was designed to systemically identify and annotate the shared susceptibility genes between IgAN and SLE. We first conducted an imputation-based genome-wide association analysis in 1180 IgAN cases and 899 controls, 1639 SLE cases and 2410 controls. Then we integrated blood expression quantitative trait loci (eQTL) databases and gene expression data to prioritize the potentially functional genes. The results showed that a total of 1928 SNPs mapping to 14 loci were identified to be shared genes between IgAN and SLE. Conditional analysis prioritized 18 independent SNPs, among which alleles of 4 SNPs in HLA and 7 SNPs in non-HLA loci were risk for SLE were protective alleles for IgAN. Most of the shared SNPs and their proxies (r2 ≥ 0.8 in Asians) (181/184, 98.37%) in non-HLA loci were located in non-coding regions. By analyzing two publicly independent blood-eQTL databases, four genes UBE2L3, FCGR2B, ANXA6, and BLK, which seemed to be restricted to PBMC or its subsets were prioritized. Among them only UBE2L3 showed consistent direction between SLE and IgAN, while the others showed opposite directions. Differential gene analysis showed that UBE2L3 was highly expressed in both SLE and IgAN, while FCGR2B and BLK showed marginal significance in SLE and IgAN, respectively. By exploring the pleiotropy of shared genes between IgAN and SLE, our results provide important clues for understanding the shared role of plasmablasts but the distinct role of B cells in pathogenesis of these two diseases.

1,180 East Asian ancestry cases, 899 East Asian ancestry controls

Chapter III

Study Statistics

Key metrics and study information

2079
Total Participants
GWAS
Study Type
No
Replicated
East Asian
Ancestry
China, Hong Kong SAR
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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Analysis In Progress

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