摘要
Background： Systemic lupus eiLythenaatosus （SLE） is a prototypic autoimmune disease wida complex genetic inheritance. This study was conducted to examine whether the association ofa proliferation-inducing ligand （APRIL）, spermatogenesis associated 8 （SPATA8）, platelet-derived growth lhctor receptor-alpha （PDGFRA）, and DNA polymerase beta （POLB） with SLE can be replicated in a Chinese Han population. Methods： Chinese SLE patients （n = 1247） and ethnically and geographically matched healthy controls （n 1440） were genotyped for the APRI L, SPATAS. PDGFRA, and POLB single-nucleotide polymorphisms （SN Ps）, rs3803800 rs8023715, rs1364089 and rsl2678588 using the Sequenom MassARRAY System. Results： The Chinese Hart SLE patients and controls had statistically similar liequencies of alleles and genotypes of four gene polynlorphisms. Moreover, no association signal was detected on different genetic models （additive, dominant, and recessive, all, P〉 0.05） or in SLE subgroups stratified by various clinical nlanifestations （all, P 〉 0.05）. Conclusions： Different genetic backgrounds from different ancestries and various populations may result in different genetic risk litctors for SLE. We did not detect any significant association with SNPs of APRIL SPATAS, PDGFRA, and POLB.
Background： Systemic lupus eiLythenaatosus （SLE） is a prototypic autoimmune disease wida complex genetic inheritance. This study was conducted to examine whether the association ofa proliferation-inducing ligand （APRIL）, spermatogenesis associated 8 （SPATA8）, platelet-derived growth lhctor receptor-alpha （PDGFRA）, and DNA polymerase beta （POLB） with SLE can be replicated in a Chinese Han population. Methods： Chinese SLE patients （n = 1247） and ethnically and geographically matched healthy controls （n 1440） were genotyped for the APRI L, SPATAS. PDGFRA, and POLB single-nucleotide polymorphisms （SN Ps）, rs3803800 rs8023715, rs1364089 and rsl2678588 using the Sequenom MassARRAY System. Results： The Chinese Hart SLE patients and controls had statistically similar liequencies of alleles and genotypes of four gene polynlorphisms. Moreover, no association signal was detected on different genetic models （additive, dominant, and recessive, all, P〉 0.05） or in SLE subgroups stratified by various clinical nlanifestations （all, P 〉 0.05）. Conclusions： Different genetic backgrounds from different ancestries and various populations may result in different genetic risk litctors for SLE. We did not detect any significant association with SNPs of APRIL SPATAS, PDGFRA, and POLB.
基金
the grant from the National Natural Science Foundation of China
