THU0348 IDENTIFICATION OF CIRCULATING CELLS WITH AN HYBRID M1/M2 MACROPHAGE PHENOTYPE IN SYSTEMIC SCLEROSIS PATIENTS AND CORRELATIONS WITH SELECTED CLINICAL ASPECTS

Background: Systemic sclerosis (SSc) is characterized by immune system alterations, vascular damage and fibrosis (1). Macrophages seem to have an emerging role in SSc, and the characterization of their polarized phenotype, starting from the dichotomic definition of classically activated (M1) or alternatively activated (M2) macrophages, is a recent research topic of interest (2). Objectives: The study investigated a possible imbalance in the distribution of circulating cells expressing M1 and M2 markers in SSc patients (pts) compared to healthy subjects (HSs), and the presence of circulating cells co-expressing M1 and M2 surface markers. Possible correlations between their percentage and selected SSc clinical aspects were investigated. Methods: In the study 55 SSc pts (50 females/5 males, mean age 64±13 yrs), fulfilling the new EULAR/ACR criteria for SSc diagnosis, and 27 age-matched HSs (25 females/2 males, mean age 57±7 yrs) were enrolled after written informed consent. Nailfold videocapillaroscopy (NVC), evaluation of SSc-related antibodies and pulmonary functional tests were performed. In particular, circulating cells belonging to the leukocyte and monocyte populations (CD45+and CD14+cells) were investigated by flow cytometry (FC) using the surface markers characterizing M1 (CD80, CD86, TLR2, TLR4) and M2 phenotypes (CD204, CD206, CD163). Statistical analysis was performed using Mann-Whitney and Kruskal-Wallis tests, and correlations were explored by bivariate Pearson’s analysis. Results: Increased circulating cells showing an M2 phenotype and characterized as CD204+CD206+CD163+cells was observed in SSc pts compared to HSs (p Conclusion: The study identified a circulating cell population expressing both M1 and M2 surface markers, which is increased together with circulating M2 cells in SSc pts, in particular affected by ILD and high PAP, suggesting their possible involvement in the pathogenesis of those disease complications. Further evaluations are in progress. References: [1] Cutolo M, et al. Nat Rev Rheumatol. 2015;11:569-71. 2. Stifano G, et al. Curr Rheumatol Rep. 2016;18:2. Disclosure of Interests: None declared