Ic markers FoxP3 and IL-10. Summary/Conclusion: These data show that exosomal signalling of PTS resident cells is controlled by pore size, therefore influencing T cell differentiation and host response. Especially, exosomes from cells in one hundred PTS proportionally upregulate T cell markers connected with Th1, Th2 and Th3 T cell subpopulations and transcriptomic stimulation, whereas exosomes from 40 PTS induce a proportional upregulation of T cell markers associated with immunomodulatory Tregs, with no broad transcriptomic stimulation. Our subsequent experiments will examine the potential of exosomes generated in 40 PTS to recapitulate a healing response in implants identified to otherwise market the foreign body response.PF01.Immunomodulatory exosomal signalling mediated by porous templated scaffolds Thomas Hady, Billanna Hwang and James Bryers University of Washington, Seattle, USAPF01.Extracellular vesicles in systemic sclerosis as possible mediator for pulmonary vascular disease Federica Rotaa, Alessandro Albinib, Marco Vicenzib, Rosa Casellab, Santaniello Alessandrob, Lorenzo Berettab, Jacopo Marianic, Laura Cantonea, Laura Dionia, Valentina Bollatic and Federico Lombardiba EPIGET LAB, Division of Clinical Sciences and Neighborhood Well being, Universitdegli Studi di Milano, Milan, Italy; bFondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico, Milan, Italy; cUniversity of Milan, Department of Clinical Sciences and Neighborhood Overall health, Milan, ItalyIntroduction: Porous templated scaffolds (PTS) with pores 40 in diameter drive healing upon implantation by lowering inflammation and foreign physique rejection while increasing regional angiogenesis. Macrophage recruitment and polarization are recognized to play roles within this CD233 Proteins Biological Activity phenomenon, however the mechanism driving this healing response is poorly understood. We think 40 PTS resident immune cells are releasing exosomes containing one of a kind cargo that modulates healing by influencing CD4+ T cell subsets. Techniques: We quantified the cellular origin and internal composition of exosomes isolated from Siglec-5/CD170 Proteins supplier explanted 40 and 100 PTS employing a Cre-Lox double transgenic mouse model and qPCR, respectively. We then quantified the cellular response to these exosomes in vitro using qPCR, ELISA and cell proliferation assays.Introduction: Pulmonary vascular disease (PVD) is characterized by media muscular hypertrophy/hyperplasia. Lately, the deregulation of EVs in some types of pulmonary hypertension research has been reported, but information on pulmonary vascular illness are still lacking. We investigated regardless of whether EVs from SSc patients with or without the need of established PVD can induce hypertrophy and/or hyperplasia in in vitro smooth muscle cells and to study vesicular miRNAs expression. Approaches: We isolated plasma EVs from: three SSc-PAH patients with established PVD below target therapy [PH+]; three SSc sufferers with higher clinical danger devoid of PVD [PH-]; 3 early SSc patients with low clinical riskISEV2019 ABSTRACT BOOK[Ea]; and three healthy control subjects. Smooth muscle cells have been cultured in RPMI complete medium enriched with EVs purified from every single study subject. Real-time cell development was analysed with xCELLigence RTCA. miRNAs from both plasma and medium cell EVs had been characterized and target prediction was performed by means of Diana Tools mirPath two.0. Results: Real-time evaluation of cellular growth showed a brisker development in every aliquot exposed to EVs with respect to the control. The intergroup comparison showed that EVs from controls induced an inferior gr.