Journal
RHEUMATOLOGY INTERNATIONAL
Volume 41, Issue 12, Pages 2205-2213Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00296-021-04996-z
Keywords
Systemic lupus erythematosus; Lupus nephritis; Interleukin-17; Receptors; Transforming growth factor beta1; Single nucleotide polymorphism
Categories
Funding
- [D-67/2016]
Ask authors/readers for more resources
This study found an association between TGFB1 gene polymorphism and SLE, and suggested that variations in IL-17A and IL-17RC genes may be related to the clinical manifestations of SLE. The IL-17A serum levels did not show significant differences between SLE patients and healthy controls, but a weak correlation with SLEDAI-2K was observed.
Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease and polymorphisms in the cytokine genes and their receptors are thought to influence its development. The aim of this case-control study was to investigate the association of the IL-17A rs2275913, IL-17RC rs708567 and TGFB1 rs1800469 polymorphisms with SLE, its clinical manifestations and the polymorphisms influence on the IL-17A serum levels. Altogether 59 SLE patients with lupus nephritis and 95 healthy controls were genotyped by TaqMan assay. Serum levels were determined by Human IL-17A Platinum ELISA kit. From the studied polymorphisms, only TGFB1 T allele was found to be associated with SLE. Within the patient group, IL-17A GG genotype and TGFB1 -509T allele showed an association with the neurological disease and IL-17RC CC genotype appeared to be associated with lupus arthritis. The IL17A serum levels in the SLE and control groups (7.24 pg/ml and 5.76 pg/ml, respectively) did not show any statistical difference. A weak correlation between IL17A levels and SLEDAI-2K was observed. Our results indicate that IL-17A rs2275913, IL-17RCrs708567 and TGFB1 rs1800469 polymorphisms might play a role in the susceptibility and the clinical manifestations of SLE and IL-17A serum levels should be monitored in the course of the disease. The identification of subsets of SLE with an IL-17-driven disease could improve the therapeutic approach leading to more precise personalized treatment.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available