Rheumatology (Oxford, England) · 2026
Disease activity and anti-topoisomerase I antibody positivity are associated with elevated serum B cell activating factor levels and a B cell subset-wide reduction of BAFF-receptor expression in SSc.
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Alzahrani Abdulellah M, Neys Stefan F H, van Oostveen Wieke M, Ahmed Saad, Levarht Ew Nivine, Hendriks Rudi W, Corneth Odilia B J, Scherer Hans Ulrich, Toes Rene E M, de Vries-Bouwstra Jeska K, Fehres Cynthia M
Аннотация
OBJECTIVES: Although B cell activating factor (BAFF) serum levels are reported to correlate with the extent of skin fibrosis and markers of systemic inflammation in SSc, their relationship with BAFF-receptor (BAFF-R) expression levels and their potential as biomarker for active disease is not investigated so far. This study was undertaken to investigate BAFF/BAFF-R dynamics in SSc and how they relate to autoantibody subtype and disease activity.
METHODS: Peripheral blood mononuclear cells of 69 SSc patients (ACA+: n = 37; ATA+: n = 32) and 10 age- and sex-matched controls were stained for BAFF-R followed by flow cytometry analyses. Serum BAFF and autoantibody levels were measured by ELISA.
RESULTS: BAFF levels were significantly elevated in SSc patients compared with the controls. This was more pronounced in clinically active than clinically stable patients, and in ATA+ compared with the controls and ACA+ SSc patients. Concurrently, BAFF-R expression was reduced on total and on several B cell subsets. BAFF-R expression correlated inversely to serum BAFF levels. In addition, BAFF levels correlated with ESR and CRP in ATA+ SSc patients. Of note, we observed a moderate correlation between BAFF and ATA-IgG, but not between BAFF and ACA-IgG.
CONCLUSIONS: Our study indicates that elevated BAFF levels, coupled with a reduction in BAFF-R expression, are significant characteristics in ATA+ SSc and of clinically active patients regardless of autoantibody status. Furthermore, BAFF levels show correlations with markers of systemic inflammation and autoantibody levels, specifically in ATA+ SSc. These findings might indicate distinct regulation of B cell responses in ATA+ and ACA+ SSc, particularly emphasizing their relevance in the context of clinically active SSc.
METHODS: Peripheral blood mononuclear cells of 69 SSc patients (ACA+: n = 37; ATA+: n = 32) and 10 age- and sex-matched controls were stained for BAFF-R followed by flow cytometry analyses. Serum BAFF and autoantibody levels were measured by ELISA.
RESULTS: BAFF levels were significantly elevated in SSc patients compared with the controls. This was more pronounced in clinically active than clinically stable patients, and in ATA+ compared with the controls and ACA+ SSc patients. Concurrently, BAFF-R expression was reduced on total and on several B cell subsets. BAFF-R expression correlated inversely to serum BAFF levels. In addition, BAFF levels correlated with ESR and CRP in ATA+ SSc patients. Of note, we observed a moderate correlation between BAFF and ATA-IgG, but not between BAFF and ACA-IgG.
CONCLUSIONS: Our study indicates that elevated BAFF levels, coupled with a reduction in BAFF-R expression, are significant characteristics in ATA+ SSc and of clinically active patients regardless of autoantibody status. Furthermore, BAFF levels show correlations with markers of systemic inflammation and autoantibody levels, specifically in ATA+ SSc. These findings might indicate distinct regulation of B cell responses in ATA+ and ACA+ SSc, particularly emphasizing their relevance in the context of clinically active SSc.