Abstract
Objective: This study aimed to determine the genotype distribution of the TNFSF4 (Tumor Necrosis Factor Superfamily 4) gene rs2205960 in Systemic Lupus Erythematosus (SLE) patients in Bandung, West Java, Indonesia.
 Methods: This was a cross-sectional study; 84 genomic DNA samples were amplified, electrophoresed, then analyzed by DNA sequencing.
 Results: The genotype distribution of the TNFSF4 gene rs2205960 in SLE patients showed that from 84 DNA samples, 55 patients are GG (65.48%), 25 patients are GT (29.76%), and 4 patients are TT (4.76%).
 Conclusion: Results indicate that SLE patients in Bandung have a genotype distribution of the TNFSF4 rs2205960 gene that fulfills the Hardy-Weinberg equilibrium.
Highlights
Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disease with various clinical manifestations affecting multiple organ systems [1]
The Tumor Necrosis Factor Superfamily 4 (TNFSF4) gene encodes OX40L, a ligand for the OX40 receptor, which is a member of the tumor necrosis factor (TNF) superfamily that is expressed on antigen-presenting cells, such as B cells, dendritic cells, macrophages, mast cells, endothelial vascular cells, and natural killer cells [4,5,6,7,8]
The rejection of the null hypothesis (H0) indicates that there is a change in allele frequency from generation to generation which means that it does not fulfill the Hardy-Weinberg equilibrium, and the acceptance of H0 states that the distribution in the population is consistent with the Hardy-Weinberg equilibrium [21]
Summary
Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disease with various clinical manifestations affecting multiple organ systems [1]. SLE patients experience a loss of selftolerance due to an abnormal immunological function, which leads to the formation of immune complexes that can damage tissues and characterized by the production of autoantibodies, activation of the complement system, and the involvement of genetic and environmental components [1, 2]. The cause of SLE is very multifactorial, between various genetic and environmental factors that contribute to disease susceptibility [3]. Many studies have shown the relationship between polymorphisms of several genes with SLE susceptibility, one of which is the Tumor Necrosis Factor Superfamily 4 (TNFSF4) gene. This gene is located in chromosome 1 at position 25 (1q25). The TNFSF4 gene encodes OX40L, a ligand for the OX40 receptor, which is a member of the tumor necrosis factor (TNF) superfamily that is expressed on antigen-presenting cells, such as B cells, dendritic cells, macrophages, mast cells, endothelial vascular cells, and natural killer cells [4,5,6,7,8]
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