Tnfsf13b, also known as the gene encoding B-cell activating factor (BAFF) (tumor necrosis factor ligand superfamily member 13B), is a key regulator in the immune system. BAFF is crucial for the survival of transitional and mature B cells [3]. It is involved in maintaining the B-cell pool and humoral immunity, and its overexpression can lead to autoimmunity in mice, with elevated levels detected in the sera of autoimmune patients [3,6].

Polymorphisms in the Tnfsf13b gene are related to the susceptibility of primary Sjögren's syndrome (pSS). The SNP rs12583006 was significantly related to pSS susceptibility in pSS patients, and polymorphisms in this gene were related to vulnerability to pSS among both pSS patients and healthy controls [1]. In rheumatoid arthritis (RA), the rs9514828 T allele and the TAT haplotype were associated with an increased risk of developing the disease, and the rs9514828 (- 871 C > T) polymorphism was associated with increased gene expression in RA patients [2]. In apical periodontitis, the rs9514828 (- 871 C > T) polymorphism was associated with primary apical periodontitis (pAP) susceptibility, with the TT genotype and T allele associated with an increased risk of pAP, while the minor allele T decreased the risk of secondary AP (sAP) [4]. Also, in severe adenovirus pneumonia in pediatric patients, the protein level of Tnfsf13b in plasma was enhanced, and it showed potential as an inflammatory indicator to predict severe cases [5].

In conclusion, Tnfsf13b is essential for B-cell survival and humoral immunity. Genetic polymorphisms of Tnfsf13b are associated with various autoimmune and inflammatory diseases such as pSS, RA, and apical periodontitis. The elevation of Tnfsf13b protein levels in plasma may serve as an indicator for severe adenovirus pneumonia in pediatric patients. Understanding the role of Tnfsf13b through these genetic-based disease associations helps in further exploring the mechanisms of these diseases and potentially developing new treatment strategies.