Description of work: FOXP3+ Treg are key players in maintaining peripheral tolerance and have been presented as promising therapeutic targets in human autoimmune diseases (AID), such as Juvenile Idiopathic Arthritis (JIA). It is still not clear whether Treg numbers and/or function are impaired in chronic inflammatory diseases, and especially their suppressive capacity at the site of inflammation remains elusive. This ESR will study the mechanisms of decreased ability to suppress inflammatory Teff. He/she will focus on activation of protein kinase B (PKB)/c-akt as we recently showed that this enhanced activation in synovial fluid-derived Teff negatively influences the capacity of Treg to suppress their activity. This suggests that for a Treg enhancing strategy to be successful as a treatment, resistance of Teff to suppression should be targeted as well. This might be achieved by selectively inhibiting PKB/c-akt activation. He/she will study mechanisms involved in this increased activation in relation to Treg mediated-suppression. In addition he/she will study (in WP 2) the microenvironment at the site of inflammation, focusing on the cytokine networks and their effects on effector and regulatory T cells.Personal Information Sheet ESR02 – Alessandra PetrelliPresentation ESR02 Alessandra Petrelli |