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AB0011 HLA-DP Polymorphisms Play Protective Role in Systemic Lupus Erythematosus in Chinese Han Population
  1. Z. Junlong,
  2. Z. Wenli,
  3. T. Anning,
  4. C. Lin,
  5. Y. Bin,
  6. W. Lanlan
  1. Department of Laboratory Medicine, West China Hospital, Sichuan University, Chengdu, China

Abstract

Background With the application of Genome-Wide Association studies (GWAS), the SLE risk gene loci in HLA-DR and HLA-DQ are gradually revealed [1]. However, the association of HLA-DP polymorphisms with SLE is pretty few reported. Considering the variants in rs3077 and rs9277535 in HLA-DP region were estimated influenced the immune response by affecting antigen presentation of HLA class II molecules to CD4+ T cells [2], it is worthy to explore the role of HLA-DP polymorphisms in SLE.

Objectives Exploring the effects of presently hot HLA-DP SNPs, rs3077 and rs9277525 on SLE.

Methods 335 SLE patients and 635 healthy controls were recruited in present study. Genotyping was performed with polymerase chain reaction-high resolution melting (PCR-HRM) assay and the data was analyzed using SPSS19.0.

Results A significantly positive correlation was observed between the SNP rs3077 and rs9277535 of HLA-DP and SLE susceptibility (rs3077, OR=0.74, 95%CI=0.60–0.91, P=0.004; rs9277535, OR=0.72, 95%CI=0.60–0.91, P=0.001). Moreover, in cytokines, there was significant positive association between rs3077 and IL-17 and INF-γ(P=0.037 and P=0.020 respectively; recessive model, P=0.011 and P=0.008, respectively) and the AA genotype predisposed to lower IL-17 and INF-γcompared with other two genotypes. However, none positive connection was found between rs3077 and IL-1 alpha, IL-4, IL-6, IL-10, and IL-23 (P=0.739, 0.624, 0.685, 0.887, and 0.937 correspondingly). None significant positive correlation could be observed between rs9277535 and any cytokines.

Conclusions HLA-DP polymorphisms (rs3077 and rs9277535) play a protective role in SLE susceptibility. And rs3077 play the role by affecting antigen presentation of HLA class II molecules for CD4+T cells and down-regulating the Th17 signal pathway.

  1. Ghodke-Puranik Y, et al. J Autoimmun. 2015; 64:125–136.

  2. Kamatani Y1, et al. Nat Genet 2009;41:591–595.

Disclosure of Interest None declared

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