The article explores the association between overexpression of BAFF (B cell activating factor) and altered B cell differentiation in the development of Sjögren’s syndrome (SS). BAFF is a member of the TNF superfamily that regulates B lymphocyte proliferation and survival. In BAFF transgenic (Tg) mice, aging leads to a secondary pathology resembling SS, characterized by severe sialadenitis, reduced saliva production, and destruction of submaxillary glands. Human SS is also associated with elevated BAFF levels and increased BAFF expression in inflamed salivary glands. The study suggests that excessive BAFF signals may disrupt B cell tolerance, allowing autoreactive B cells to survive and potentially contribute to SS pathology. BAFF Tg mice exhibit enlarged marginal zone (MZ) B cell subsets, and MZ-like B cells infiltrate salivary glands, indicating their involvement in tissue damage. The study also found significantly elevated BAFF levels in SS patients compared to those with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), suggesting a more prominent role of BAFF in SS progression. The research used flow cytometry, immunohistochemistry, and ELISA to analyze B cell subsets, inflammation, and BAFF levels in BAFF Tg mice and human SS patients. Results showed that BAFF Tg mice developed a pathology similar to SS, with increased B cell infiltration and reduced saliva production. Additionally, BAFF expression was detected in lymphocytic infiltrates of SS patients, further supporting its role in SS pathogenesis. The study concludes that altered B cell differentiation and tolerance due to excess BAFF may be central to SS pathogenesis. It highlights the potential of BAFF as a therapeutic target in autoimmune diseases, including SS. The findings provide insights into the mechanisms underlying SS and suggest that targeting BAFF or its signaling pathways could offer new treatment strategies for this condition.The article explores the association between overexpression of BAFF (B cell activating factor) and altered B cell differentiation in the development of Sjögren’s syndrome (SS). BAFF is a member of the TNF superfamily that regulates B lymphocyte proliferation and survival. In BAFF transgenic (Tg) mice, aging leads to a secondary pathology resembling SS, characterized by severe sialadenitis, reduced saliva production, and destruction of submaxillary glands. Human SS is also associated with elevated BAFF levels and increased BAFF expression in inflamed salivary glands. The study suggests that excessive BAFF signals may disrupt B cell tolerance, allowing autoreactive B cells to survive and potentially contribute to SS pathology. BAFF Tg mice exhibit enlarged marginal zone (MZ) B cell subsets, and MZ-like B cells infiltrate salivary glands, indicating their involvement in tissue damage. The study also found significantly elevated BAFF levels in SS patients compared to those with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), suggesting a more prominent role of BAFF in SS progression. The research used flow cytometry, immunohistochemistry, and ELISA to analyze B cell subsets, inflammation, and BAFF levels in BAFF Tg mice and human SS patients. Results showed that BAFF Tg mice developed a pathology similar to SS, with increased B cell infiltration and reduced saliva production. Additionally, BAFF expression was detected in lymphocytic infiltrates of SS patients, further supporting its role in SS pathogenesis. The study concludes that altered B cell differentiation and tolerance due to excess BAFF may be central to SS pathogenesis. It highlights the potential of BAFF as a therapeutic target in autoimmune diseases, including SS. The findings provide insights into the mechanisms underlying SS and suggest that targeting BAFF or its signaling pathways could offer new treatment strategies for this condition.