Gewählte Publikation:
Prietl, B.
The role of regulatory immune cells in autoimmunity and immune tolerance in type 1 diabetes
PhD-Studium (Doctor of Philosophy); Humanmedizin; [ Dissertation ] Graz Medical University; 2016. pp.
[OPEN ACCESS]
FullText
- Autor*innen der Med Uni Graz:
-
Prietl Barbara
- Betreuer*innen:
-
Pieber Thomas
-
Strunk Dirk
-
Treiber Gerlies
- Altmetrics:
- Abstract:
- The immune-suppressive function of regulatory T cells (Tregs) is essential for maintaining immunological self-tolerance. The role of Tregs in autoimmune diseases, such as type 1 diabetes mellitus (T1D), is not fully understood yet. Reports from animal and in-vitro models suggest a pivotal role for Tregs in the pathogenesis of autoimmunity. In T1D treatment, vitamin D has been found to modulate Tregs and to correct auto-immune processes in animal models for T1D. Another treatment option could be based on glucagon-like peptide-1 (GLP1) which was recently described to interfere with inflammatory pathways involved in T1D. In five clinical studies performed within this thesis the role of Tregs and other peripheral immune cells in T1D was investigated and supplementation therapies, aiming to increase the percentage or the functional capacity of regulatory immune cells were performed. The characteristics of Tregs and other peripheral immune cells were mainly assessed by multi-parameter FACS analysis, quantitative real time PCR and ex-vivo co-cultures. The results of this thesis provide significant new information about the differences in peripheral immune-cell characteristics between healthy conditions and T1D and support the findings about the potential role for vitamin D therapy as a mechanism in controlling autoimmunity by restoring Tregs. Obtained data about the GLP1-receptor distribution on human peripheral immune-cells and the response of healthy participants to GLP1-receptor-agonist treatment provide a rationale for future trials, testing the complementary effect of vitamin D in combination with GLP1R-therapies in the context of T1D and other autoimmune diseases.