Session Title: Sjögren's Syndrome - Pathogenesis
Session Type: Abstract Submissions (ACR)
B cells have traditionally been considered as positive regulators of humoral immune response, however their negative regulatory role has recently being recognized. Objective. To characterize the phenotypes of regulatory B cells in peripheral blood of primary Sjögren syndrome (pSS) patients and compare their presence according to the clinical and/or serologic activity disease status.
Methods: We included 50 pSS patients according to the AECG classification criteria, all of them were evaluated by a rheumatologist. We defined clinical activity as the presence of parotid enlargement or any extraglandular manifestation assessed by the SDAI or the ESSDAI indexes (except fatigue, fever or arthralgias). We defined serologic activity as IgG immunoglobulin >16 g or low C3, C4 or serum viscosity >1.9 cp. Twelve healthy age matched subjects were used as controls. PBMCs were isolated by centrifugation over a Lymphoprep gradient. CD19-mAb-coated microbeads were used to purify B cells by positive selection. We used the following mAbs: anti-CD38-PECy5, anti-CD38-PE, anti-CD24-FITC, anti-IgA-PE, anti-IgD-PE, anti-IgG-PECy5, anti-IgM-APC, anti-CD5-APC, anti-CD10-APC, anti-CD20-APC, anti-CD27-APC, anti-CXCR4-APC and anti-CXCR7-Cy5. Cells immunofluorescent staining was analyzed by a FACScalibur flow cytometer. The relative % of the subtypes of Il-10 cells producers was calculated on basis of the total positive selection of the phenotype CD19+/CD38bright/CD24bright. We used One way ANOVA analysis (post-hoc analysis Dunn method) with the Sigma Stat 11.2 software.
Results: Patients were predominantly females, mean age 53±12 years and median disease duration of 9.7 years. Seventeen patients (34%) were clinical active (parotid enlargement, vasculitis, arthritis, leucopenia, lymphopenia, pneumonitis or optic neuritis). Patients with or without clinical activity were similar in age, disease duration but received more frequently prednisone and azathioprine. Twenty-seven (54%) patients had serologic activity regardless their clinical status. IL-10+ B cells represented the 0.55% of the total pSS B cell population and was higher in clinical inactive patients(0.63%), whereas controls had a lower prevalence (0.22%, p<0.05). We found a statistically significant increment in the following subtypes of Bregs cells: CD19+/CD38bright/IgA+/IL10+ cells (pSS 79%, clinical inactive 80% vs. control 66%), CD19+/CD24bright/CD38bright/CD5+/IL10+ (clinical inactive 24% vs. control 14%), CD10+/IL10+ (pSS 23%, clinical inactive 26% vs. control 15%). IgD+ cells and CD27–/IL10+ cells were increased in all the groups regardless their clinical activity when compared vs. controls. The phenotypes CD19+/CD24bright/CD38brightIL10+/CD20+, CD27+, CXCR4+ and CXCR7+ were similar among groups. We did not find a difference when we analyzed by serologic activity.
Conclusion: Most of the studied Bregs phenotypes were increased in pSS patients, particularly in those without clinical activity. The presence of these cells emphasizes the importance of the immunobiology of B cells in pSS.
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