Type 1 Diabetes (T1D) is an autoimmune disease with continuously increasing incidence and worldwide distribution. The onset of T1D in Caucasians is predominantly in childhood between 5 and 15 years, however, T1D patients from Sub-Saharan Africa have a delayed disease onset. Differences in age of onset are largely associated with genetic factors; polymorphisms of class II HLA genes encoding DQ and DR account for familial aggregation of T1D. However, previous studies have demonstrated a low concordance rate of T1D susceptibility in monozygotic twins raising concerns about the influence of environmental factors including infections and vaccination. Nevertheless, the underlying immune pathology, potentially influential environmental factors, and the precise cause of T1D onset are poorly defined so far. Aberrant effector and regulatory T cell activity have been observed in T1D patients. An increased effector and a reduced regulatory T cell function led to infiltration of autoreactive CD4+ T cells around the pancreatic islet β cells, eventually causing their destruction and loss of function. To date, there is a lack of established evidence of T cell-related differences between early and late-onset T1D.
This project aims to investigate the role of differential immune pathology and external factors for early or late T1D onset in patient cohorts from Ghana and Germany. This will enable us to identify biomarkers of immune pathology and influential external factors contributing to differences in the early onset age in German T1D patients as well as to the delayed T1D onset in Ghana.
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