Tumor Necrosis Factor Superfamily Member 15 (TNFSF15) rs4979462 Variant and TNFSF15 serum levels evaluation in systemic lupus erythematosus

Background and objectives

Tumor necrosis factor (TNF) superfamily member 15 (TNFSF15) may have the potential to control vascular homeostasis and inflammation. Through binding to death receptor 3 (TNFRSF25), TNFSF15 promotes T-cell activation, proliferation, and the generation of multiple cytokines. TNFSF15-TNFRSF25 signaling is essential for effective T-cell immune responses in T-cell-mediated autoimmune diseases. Our goal is to study the role of the (TNFSF15) rs4979462 gene variant and TNFSF15 serum levels in systemic lupus erythematosus (SLE) in Egyptian patients.

Methods

A total of 118 patients with SLE and 102 age- and sex-matched healthy control volunteers were genotyped for the TNFSF15 rs4979462 variant by polymerase chain reaction-restriction fragment length polymorphism and verified by direct sequencing. TNFSF15 serum levels were measured using an enzyme-linked immunosorbent assay.

Results

Regarding the TNFSF15 rs4979462 gene variant, there was a significant increase in the frequencies of combined genotypes (CT + TT) and T-allele among female patients with SLE compared with the healthy female subjects (OR = 2.6, 95% CI = 1.1–6.3, p = 0.027; OR = 2.7, 95% CI = 1.2–6.3, p = 0.015, respectively). The T-variant was significantly associated with serositis and thrombotic manifestations (OR = 2.8, 95% CI = 1.1–7.1, p = 0.032; OR = 2.9, 95% CI = 1.1–7.8, p = 0.023, respectively). The median serum TNFSF15 concentration was significantly higher in patients with SLE compared to the healthy control group and was correlated with the disease activity (p = 0.023, 0.012, respectively).

Conclusions

The TNFSF15 rs4979462 gene variant increases the risk of SLE in female subjects and modulates the clinical outcome of the disease. TNFSF15 serum level could be a biological marker of SLE disease activity.

Full text

https://www.xiahepublishing.com/1555-3884/GE-2023-00060

The study was recently published in the Gene Expression.

Gene Expression (GE) is an open-access journal. It was launched in 1991 by Chicago Medical School Press, and transferred to Cognizant Communication Corporation in 1994. From August 2022, GE is published by Xia & He Publishing Inc.   

GE publishes peer-reviewed and high-quality original articles, reviews, editorials, commentaries, and opinions on its primary research topics including cell biology, molecular biology, genes, and genetics, especially on the cellular and molecular mechanisms of human diseases. 

GE has been indexed in Medline (1991-2021), Scopus, Biological Abstracts, Biosis Previews, ProQuest, etc.

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