Journal
ARTHRITIS AND RHEUMATISM
Volume 63, Issue 11, Pages 3487-3492Publisher
WILEY-BLACKWELL
DOI: 10.1002/art.30595
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Funding
- Shenzhen Science and Technology Project
- Leading Academic Discipline Program
- 211 Project for Fudan University
- National Natural Science Foundation of China
- National Natural Science Foundation of Guangdong Province
- Program for Changjiang Scholars and Innovative Research Teams in Universities [U0932004, IRT0965]
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Objective. Systemic lupus erythematosus (SLE) represents the classic prototype of systemic autoimmune disease. The identification of the Th17 cell subset has provided new understanding regarding the underlying mechanisms of autoimmunity. Copy number variations (CNVS) have been discovered to have phenotypic consequences and are associated with various types of diseases. We undertook this study to explore a possible association between CNVS of Th17 cell-related genes and the risk of SLE. Methods. We extracted genomic DNA and RNA from 938 SLE patients and 1,017 healthy controls. We examined CNVS of Th17 cell-related genes, including retinoic acid receptor-related orphan nuclear receptor gamma t, STAT-3, interleukin-6 (IL-6), transforming growth factor beta, tumor necrosis factor alpha, IL-17A, IL-17F, IL-21, IL-22, IL-23A, CCL20, and CCR6, and levels of messenger RNA (mRNA) for IL-17F, IL-21, and IL-22. Results. Genotype and allele frequencies for copy number amplifications of IL-17F, IL-21, and IL-22 were found to be significantly higher in SLE patients than in healthy controls. CNVS of IL-17F, IL-21, and IL-22 had no synergistic contribution to SLE. The mRNA expression of IL-17F, IL-21, and IL-22 in the samples with >2 copies of DNA was significantly higher than that in those with 2 copies of DNA. Conclusion. Our findings indicate that CNVS of IL-17F, IL-21, and IL-22 are associated with the risk of SLE.
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