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Presentation/PPT
27/08/2022
What are the initiating factors?
Are viruses involved? Are these unique or common?
Are any of these factors intrinsic to -cells in T1D patients?
Which antigens are presented, and does this change over time or in different patients?
How does the microbiome affect the induction or progression of autoimmunity?
How are innate responses involved?
What is the role of epigenetic changes in the penetrance of disease?
How does the immune repertoire differ in patients who will develop T1D?
What is the antigen specificity of pathogenic T cells, and how can these cells be identified?
How much of the disease heterogeneity stems from stochastic variation in immune development versus exposure to
natural pathogens versus normal responses to ones environment?
Why does it take so long to destroy all of the -cells?
Are there unusual features of autoreactive T cell development pathways?
How do immune response and other genes affect disease in general or the diabetogenic potential of T cells specifically?
What is the role of cell-intrinsic regulatory mechanisms?
What are the roles of thymus-derived and peripherally induced regulatory T cells?
What are the mechanisms of -cell death?
Which cells are involved?
Do human -cells regenerate, differentiate or divide, and does this differ in very young children versus adults?
Can -cell regeneration, transdifferentiation or division be induced?
Why is -cell death segmental and in a lobular distribution?
How can treatment be improved?
What are the appropriate and realistic parameters for determining success in a clinical trial with a given modality (for
example, should restoration of -cell function be an expected outcome with a therapy that targets the autoimmune
response if -cell regeneration, transdifferentiation or division does not occur)?
What are the mechanisms of long-term failure?
Does the long-term failure of therapies reflect recurrence of the autoimmune response or failure of -cells
independently of immune attack?
How does metabolic control affect responses to immune therapies?
How can responders and non-responders be identified?
When should interventions be initiated?
Can any of the interventions prevent T1D?
What combinations are optimal, and how can the regulatory path for the development of these combinations be optimized?
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