 Salome de Pinho © ECCO |
Aims of the research
The current therapeutic strategies for Inflammatory Bowel Disease (IBD) are limited by effectiveness and/or toxicity, and the selection of patients for therapy remains a major challenge. These clinical concerns highlight the unmet need to identify key mechanisms (molecular markers) capable of being selectively targeted with new and optimised therapies. Glycosylation is a major post-translational mechanism characterised by the addition of carbohydrate structures (glycans) to essentially all cells [1]. Evidence in other immune-mediated disorders has shown that protein N-glycosylation, particularly branched N-glycans, regulates T cell immune response and controls the threshold of T cell activation [2].
