P024 Effects of anti-TNF and anti-interleukins 12 and 23 drugs on circulating dendritic cells migratory capacity in inflammatory bowel disease

Abstract Background Inflammatory bowel disease (IBD) is an idiopathic and chronic disorder that includes ulcerative colitis (UC) Crohn’s (CD). Both diseases are different but show uncontrolled intestinal immune response generates tissue inflammation. Dendritic cells (DC) phagocytic professional antigen presenting link the innate adaptive systems. Indeed, they only cell type able to stimulate naïve T generating antigen-specific response. In humans, DC can be divided into plasmacytoid (pDC) c conventional 1 2 (cDC1, cDC2). Although cDC migration towards GI mucosa enhanced in IBD, mechanisms underlying these migrations whether biological drugs modulate them currently unknown. This study aimed analyze migratory capacity mucosa, with of action this process health IBD. Methods a cross-sectional observational postmarketing where modulatory effect treatments on samples from patients endoscopic diagnosis IBD healthy controls was studied ex vivo. Peripheral blood mononuclear (PBMC) were obtained 15 per group cultured presence golimumab or ustekinumab. Following culture, surface markers expression determined, assessing differential (if any) over subsets groups. After that, circulating CCL2, CCL25, MadCam1 groups determined. Finally, we evaluated capacities culture media alone. Results The cCD2 subset showed higher levels β7 CCR5 compared cCD1 (Figure 1). Golimumab ustekinumab did not modify homing any 2). Even though no conclusive results for used markers, decreased cDC2 CD medium supplemented CCL25 3). Conclusion more profile than other populations. group. Nevertheless, patients. fact indicates behavior population UC dependent markers.