Background

T1D is a chronic, autoimmune disorder in which the insulin producing beta cells in the pancreatic islets are destroyed by an auto-immune attack. The immune attack on the beta cells is triggered by the presentation of islet-derived peptide antigens to CD4+ T‑cells by MHC Class II molecules, mostly HLA-DQ8. Every year ~30,000 new cases are diagnosed, 50% of whom are children. Recent studies demonstrate a strong association between DQ8 based antigen presentation and the development of T1D. Indeed, DQ8 has been shown to present antigenic peptides (such as InsB:9-23, GAD65) to CD4+ T‑cells leading to the destruction of the pancreatic β-cells and development of T1D. Currently there is no curative therapy for T1D, and the only available treatment is