1. Introduction
Primary Sjogren’s syndrome (pSS) is a chronic autoimmune disorder characterized by lymphocytic infiltration of exocrine glands, most notably the salivary and lacrimal glands, resulting in oral and ocular dryness. The syndrome is identified by B-cell hyperactivity, which is characterized by hypergammaglobulinemia and a variety of autoantibodies, with BAFF or BLyS, a B cell survival factor, playing a significant role.1 However, the pathogenesis and etiology of pSS are yet unknown. As a result of ongoing research, anti-Ro/SSA autoantibody has emerged as one of the most well-established risk factors for pSS, with a high correlation. Whereas, anti-Ro/SSA autoantibodies lack specificity, and studies are increasingly showing that high expression of the B-cell activating factor (BAFF) gene is also responsible for pSS.1–36
TNF ligand superfamily member 13B (TNFSF13B) is a cytokine that belongs to the TNF ligand family. It is also known as B-cell activating factor (BAFF) or B Lymphocyte Stimulator (BLyS). BAFF aids B cell proliferation, maturation, differentiation, and immunoglobulin synthesis.2 This cytokine is encoded by the TNFSF13B gene, and various single-nucleotide polymorphisms have been linked to vulnerability to various autoimmune diseases.8
Previous data suggested that TNFSF13B genotype and allele polymorphisms are involved in pSS. A study showed that the same genotype influences pSS vulnerability in both the co-dominant and recessive models. The TTTAC haplotype was discovered to enhance pSS susceptibility.2 The other showed that TNFSF13B mRNA expression was observed to be higher in rheumatoid arthritis (RA) and pSS patients. RA patients had 2.43-fold higher TNFSF13B mRNA expression than HC patients, while pSS patients had 5.04-fold higher TNFSF13B mRNA expression.3 Another research suggested that the CTAT haplotype increases disease susceptibility for Ro/La-positive pSS, but is not linked with high serum BAFF (s-BAFF) levels. Elevated s-BAFF levels in pSS are linked to the TTTT genotype and could be a secondary effect in Ro/La-positive pSS.25 In addition, the research has shown that distinct haplotypes of the BAFF gene give greater susceptibility to pSS development, and the importance of genetic polymorphisms in the BAFF gene in the development of pSS and the development of pSS-related lymphomagenesis was also highlighted.1
Although research concluded that both a genetic propensity to pSS and a specific pattern of antibody production are unrelated to the polymorphism in the BAFF gene; the study only looked at the BAFF -871 T/C polymorphism.37 Therefore, in this work, we attempted to conduct a meta-analysis for the first time to assess the relationship between pSS susceptibility and TNFSF13B gene polymorphisms.