POS0452 ABNORMALITY OF TYPE I INTERFERON SIGNALLING IN B CELLS IN PRIMARY SJÖGREN´S SYNDROME AND THE IMPACT ON LABORATORY AND CLINICAL FINDINGS

Background B cell hyperactivity (1), autoantibody production (anti-SS-A, anti-SS-B) and hypergammaglobulinaemia as well interferon (IFN) signature (2) play a central role in the pathogenesis of primary Sjögren´s Syndrome (pSS). The link between these hallmarks is still elusive. While treatment pSS remains limited, an improved understanding IFN JAK/STAT signalling on cells may hold promise to improve potential targets related biomarkers. Objectives To investigate downstream molecules pathway their clinical impact pSS. Methods Peripheral blood from 47 patients 36 matched healthy controls (HC) was obtained permeabilized for intracellular staining. Here T markers were applied together with Signal Transducers Activators Transcription 1 (STAT1), STAT2, pSTAT1 2, Interferon Regulatory factor 9 (IRF9), IRF7 IRF1 analysed by using flow cytometry. Cell subsets correlations all information subjected statistical analyses. Results Compared HC group showed significantly elevated STAT1 expression among (p>0.0001) including naïve (CD27-IgD+), pre-switched (CD27+ IgD+), switched-memory (CD27+IgD-), double negative (CD27- IgD-) plasmablasts (CD27++ CD38++). Furthermore, IRF9 STAT2 increased most subsets. Positive found Siglec-1 (CD169), marker expressed surface CD14+ monocytes (p>0.0001; r=0.633). Notably, levels positively correlates STAT1. Upregulated within associated extraglandular manifestations, high anti-SS-A anti-SS-B autoantibodies, anti-nuclear antibody titers (ANA) rheumatoid factors (IgA, IgM) patients. Patients treated prednisolone dose dependent inverse naïve-, memory-, suggesting its responsiveness. Conclusion current data provide evidence type I Elevated STAT1, suggest transcriptionally activity, which evident manifestations serologic activity. Targeting could be beneficial leading personalized approach this specific subgroup References [1]Nocturne G, Mariette X. Sjögren syndrome. Nature Reviews Rheumatology. 2018;14(3):133-45. [2]Brkic Z, Maria NI, Helden-Meeuwsen CGv, Merwe JPvd, Daele PLv, Dalm VA, et al. Prevalence CD14 Sjögren’s syndrome association disease activity BAFF gene expression. Annals Rheumatic Diseases. 2013;72(5):728-35. Disclosure Interests None declared.