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.