AB0649 PERIPHERAL B CELLS IMMUNOPHENOTYING IN SYSTEMIC LUPUS ERYTHEMATOSUS PATIENTS

Background B cells play a central role in systemic lupus erythematosus (SLE) pathogenesis connecting innate with adaptative immunity. Objectives To investigate the peripheral blood cell phenotype cohort of SLE patients renal (LN-SLE) and non-renal (NR-SLE) involvement compared to healthy controls. Methods Ninety-nine patients, 76 active (30 at disease onset-Early 46 whom LN occurred after onset-Long) 23 (articular and/or cutaneous) were enrolled. Thirty-seven controls included. Clinical, laboratory demographic data collected baseline 6 12 months follow-up. Disease activity was recorded using SLEDAI-2K. The memory immunophenotyping (IgD/CD27 classification) analyzed through flow cytometry. clarify key molecules activation, IL-6 BAFF serum levels assayed by Enzyme-linked immunosorbent assay (ELISA). Results Studying subsets, lower percentage CD19 pos unswitched (IgD CD27 ) whole (8.7±6.8% vs 10.5±3.5%; p=0.002 10.7±13.7% 15.3±8.0%; p < 0.01, respectively) observed. In addition, we found higher double-negative neg plasmablasts (CD27 CD38 than [(CD27 IgD 10.3±8.3% 4.1±1.9%; p<0.01 6.1±7.9% 1.0±0.5%; 0.01 )]. Furthermore, negatively correlated (R=-0.322; p=0.01 ). No correlation between subsets parameters. According organ involvement, LN-SLE RN-SLE showed , plasmacells [(CD19 : LN-SLE:9.1±7.4% 10.5±4.6%; p=0.005; NR-SLE: 7.7±4.6%; p=0.008 )(IgD :LN-SLE 10.4±14.9% 0.001; 11.8±8.6%; p=0.006 7.5±8.4% 0.9±0.5%; 1.6±2.2%; = 0.001 10.6±8.5% 9.6±7.3%; ]. onset symptoms, there no differences distribution classes chronicity indexes two groups. Analyzing Long-LN-SLE (8.6±6.5% p=0.004 9.7±6.9% p=0.001, (12.1±8.4%) Early (8.3±8.3%;p =0.027 ), NR-SLE (9.6±7.3%;p =0.001 controls(4.1±1.9%;p< direct observed SLEDAI (r=0.380; p=0.004). Conclusion Data on reveals distinct subset when controls, confirming an alteration strengthening hypothesis pathogenetic played lymphocytes course LN. particular, DN which damage occurs reinforcing that these represents characteristic immune system overactivation conditions. Reference [1]Sang A, Zheng YY, Morel L Contributions pathogenesis. Mol Immunol 2014; 62 (2): 329–338 Acknowledgements: NIL. Disclosure Interests None Declared.