Journal
FRONTIERS IN GENETICS
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fgene.2020.00600
Keywords
genome-wide association study; replication; IRF3; systemic lupus erythematosus; lupus nephritis
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Funding
- Clinical Key Project of Pediatrics in Fujian and Clinical Key Project in Union Hospital
- National Key Research and Development Program of China [2017YFC0909001]
- Sanming Project of Medicine in Shenzhen [201602087]
- National Natural Science Foundation of China [81402590, 81601423, 81801636]
- Research Grant Council of Hong Kong [GRF 17146616, 17125114, HKU783813M]
- National Key Basic Research Program of China [2014CB541901]
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Systemic lupus erythematosus (SLE) is a genetically complex autoimmune disease. Despite the significant progress made in identifying susceptibility genes for SLE, the genetic architecture of the disease is far from being understood. In this study, we set to replicate a number of suggestive association signals found in genome-wide association studies (GWASs) in additional independent cohorts. Replication studies were performed on Han Chinese cohorts from Hong Kong and Anhui, involving a total of 2,269 cases and 5,073 controls. We identified a missense variant inIRF3(rs7251) reaching genome-wide significance through a joint analysis of GWAS and replication data (OR = 0.876, P = 4.40E-08). A significant correlation was observed between rs7251 and lupus nephritis (LN) by subphenotype stratification (OR = 0.785, P = 0.0128). IRF3 is a key molecule in type I interferon production upon nucleic acid antigen stimulations and may inhibit regulatory T cell differentiation. Further elucidation of the mechanism of this association could help us better understand the pathogenesis of SLE.
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