Canada has the third highest rate of Type 1 Diabetes (T1D) in the world and its incidence is on the rise. Although insulin can be used to control the disease, T1D greatly increases the probability of heart attack, stroke, blindness and limb amputation, and shortened life expectancy. Although there is widespread agreement that T1D is a complex autoimmune disease caused by multiple genetic risk factors and environmental risk factors, little research has been conducted to examine these risk factors together and to understand the way they interact to produce the disease. This project seeks to understand the genetic control of T1D in humans and rodent models, and to study the role of exposure to common intestinal bacteria in regulating immune system development and how such exposures affect the probability that persons at genetic risk of T1D will develop the disease.
We studied genome-wide interactions between genetic risk variants and defined microbial exposures in modifying T1D risk in rodent models, and established the genomic platforms and pre-clinical rodent models to evaluate gene-environment interactions in human Type 1 diabetes population-based studies. Our research goals were:
- to leverage mechanistic and genome-wide analyses in spontaneous diabetic rodents to dissect the interaction between defined genetic and environmental risk factors in progression to disease;
- to analyze the impact of gestational environment on the infant immune system and susceptibility to T1D; Our ultimate objective is to integrate these data on genetic polymorphisms, immune function, exposure to intestinal microorganisms during gestation and early childhood to identify risk factors in T1D that are amenable to therapeutic intervention strategies.