SOURCE-LINKED INTELLIGENCE

ENTEROVIRUS-LINKED TYPE 1 DIABETES EXPOSED -MECHANISMS AND PREVENTION

CORDIS · observation · Publication date unknown

pe 1 diabetes (T1D), a robust association without proof of causality. Causality is addressed by a multidisciplinary, multi-layer approach, using in-vitro and in-vivo models, unique human samples, and artificial intelligence to identify mechanisms and related biomarkers, asking 3 key questions: 1. Why are only insulin-producing β-cells destroyed by EVs? Weak β-cell antiviral responses and high expression of EV entry receptors may favour EV persistence. This hypothesis is addressed using human cell models (stem-cell-derived β/α-cells, organoids, their genetic modifications, anti-EV T-cells) and pancreas tissues from T1D patients. 2. Why do only some individuals develop T1D after EV infection? Weak EV immunity may predispose to virus spreading to pancreas, persistence and local inflammation, triggering autoimmunity. This hypothesis is addressed by analysing adaptive and innate immune responses to EVs, correlating these with gene polymorphisms and EV persistence in children followed from birth and who developed T1D. 3. How can EV-associated T1D risk be attenuated? By using vaccines in

Read original source ↗ Open in workspace

recordType

award

status

SIGNED

region

EU

value

7144790

unit

EUR