1. CCL3L3-null status is associated with susceptibility to systemic lupus erythematosus.
- Author
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Kim YH, Lee EE, Sim HW, Kang EK, Won YH, Lee DE, Hong KM, and Song YW
- Subjects
- Case-Control Studies, Female, Humans, Lupus Erythematosus, Systemic epidemiology, Male, Polymerase Chain Reaction methods, Republic of Korea epidemiology, Chemokine CCL3 genetics, DNA Copy Number Variations genetics, Genetic Predisposition to Disease, Lupus Erythematosus, Systemic genetics
- Abstract
The correlation between copy number variation (CNV) and the susceptibility to systemic lupus erythematosus (SLE) has been reported for various immunity-related genes. However, the contribution of CNVs to SLE susceptibility awaits more investigation. To evaluate the copy numbers in immunity-related genes such as TNFAIP3, TNIP1, IL12B, TBX21 (T-bet), TLR7, C4A, C4B, CCL3L1, and CCL3L3, the modified real competitive polymerase chain reaction (mrcPCR) assay was employed, and the association between the copy numbers and SLE susceptibility was analyzed in 334 SLE patients and 338 controls. CCL3L3-null status was significantly associated with SLE susceptibility (OR > 18, P < 0.0001), which remained significant by Bonferroni's correction (corrected P = 0.0007). However, the significant association between C4B low-copy status and SLE susceptibility (OR = 1.6051, P = 0.0331) became non-significant by Bonferroni's correction (corrected P = 0.3938). Except for these results, no other significant association between SLE susceptibility and copy number status in other genes was observed. The CCL3L3-null status may be a significant factor for SLE susceptibility., (© 2021. The Author(s).)
- Published
- 2021
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