Autoimmune reactions against specific human proteins may contribute to the onset and progression of diseases like multiple sclerosis (MS) and inflammatory bowel diseases (IBDs). In these diseases, autoantibodies can be found that target the myelin sheath of neurons and the intestinal epithelium, respectively. Why the immune system starts to react towards specific proteins is not fully understood and may involve changes in glycosylation. Glycans direct protein conformation, sterically hinder or enable access to peptide epitopes, and can be recognized directly as antigens.
In this project, the role of glycosylation in the autoantibody response in MS and IBDs will be explored. The results may identify specific glycosylation-dependent interactions between autoantibodies and their antigens. This will provide evidence that (altered) glycosylation plays an important role in autoantibody formation and may be useful as minimally invasive biomarkers for disease detection and monitoring.