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Type 1 Diabetes is an autoimmune disease with a dramatically increasing incidence. It results from a breakdown in immune tolerance causing the autoimmune-mediated destruction of the insulin-producing beta cells in the pancreas. We are trying to get a better understanding of the mechanisms underlying Type 1 Diabetes, to contribute to the development of immune therapies that can decelerate or even halt autoimmune progression and prevent diabetes complications.

Regulatory T cells (Tregs), which express the transcription factor Foxp3, function as key players for the maintenance of peripheral immune tolerance. We have used murine and humanized models to show that the efficient induction of Foxp3+ Tregs from naive CD4+ T cells can be achieved by the application of a strong-agonistic T cell receptor (TCR) ligand under subimmunogenic conditions.

Impairments in Treg induction and function are important contributors to autoimmune disorders such as Type 1 Diabetes. However, the cellular and molecular underpinnings promoting such impairments in Treg induction as well as the specific requirements for an efficient induction of Foxp3+Tregs in the setting of ongoing islet autoimmunity remain poorly understood especially in human Type 1 Diabetes.

To fill this knowledge gap, we aim to dissect mechanisms of aberrant immune activation that can interfere with tolerance induction during islet autoimmunity and that promote progression from islet autoimmunity to clinical Type 1 Diabetes.

The team of TDI therefore uses an integrative translational research approach combining cellular and molecular immunology with immunepharmacology. To this end, we integrate murine Type 1 Diabetes models with studies in humanized mice and focus on immune cells from non-diabetic children with ongoing islet autoimmunity or with new onset Type 1 Diabetes which offer an important resource for studying such signaling pathways involved in aberrant immune activation vs. immune tolerance.

In addition, we are using murine and humanized models to study combinatorial strategies of antigen-specific tolerance induction together with novel pharmacological approaches that can limit T cell activation which have the goal to broaden the window of application closer to the precipitation of autoimmune progression and clinical disease.

Moreover, given our strong interest in dissecting mechanisms of tissue-specific immune tolerance relevant to prevent autoimmune progression in Type 1 Diabetes we focus on the role of tissue-Tregs in inhibiting immune activation and inflammation in diabetes.

We strive to integrate these findings into understanding mechanisms of immune tolerance in diabetes with the future goal of developing innovative precision medicines aimed at the safe and specific manipulation of Foxp3+Tregs in children at risk of developing Type 1 Diabetes.

Type 1 Diabetes is an autoimmune disease with a dramatically increasing incidence. It results from a breakdown in immune tolerance causing the autoimmune-mediated destruction of the insulin-producing beta cells in the pancreas. We are trying to get a better understanding of the mechanisms underlying Type 1 Diabetes, to contribute to the development of immune therapies that can decelerate or even halt autoimmune progression and prevent diabetes complications.

Regulatory T cells (Tregs), which express the transcription factor Foxp3, function as key players for the maintenance of peripheral immune tolerance. We have used murine and humanized models to show that the efficient induction of Foxp3+ Tregs from naive CD4+ T cells can be achieved by the application of a strong-agonistic T cell receptor (TCR) ligand under subimmunogenic conditions.

Impairments in Treg induction and function are important contributors to autoimmune disorders such as Type 1 Diabetes. However, the cellular and molecular underpinnings promoting such impairments in Treg induction as well as the specific requirements for an efficient induction of Foxp3+Tregs in the setting of ongoing islet autoimmunity remain poorly understood especially in human Type 1 Diabetes.

To fill this knowledge gap, we aim to dissect mechanisms of aberrant immune activation that can interfere with tolerance induction during islet autoimmunity and that promote progression from islet autoimmunity to clinical Type 1 Diabetes.

The team of TDI therefore uses an integrative translational research approach combining cellular and molecular immunology with immunepharmacology. To this end, we integrate murine Type 1 Diabetes models with studies in humanized mice and focus on immune cells from non-diabetic children with ongoing islet autoimmunity or with new onset Type 1 Diabetes which offer an important resource for studying such signaling pathways involved in aberrant immune activation vs. immune tolerance.

In addition, we are using murine and humanized models to study combinatorial strategies of antigen-specific tolerance induction together with novel pharmacological approaches that can limit T cell activation which have the goal to broaden the window of application closer to the precipitation of autoimmune progression and clinical disease.

Moreover, given our strong interest in dissecting mechanisms of tissue-specific immune tolerance relevant to prevent autoimmune progression in Type 1 Diabetes we focus on the role of tissue-Tregs in inhibiting immune activation and inflammation in diabetes.

We strive to integrate these findings into understanding mechanisms of immune tolerance in diabetes with the future goal of developing innovative precision medicines aimed at the safe and specific manipulation of Foxp3+Tregs in children at risk of developing Type 1 Diabetes.

Contact Us

Laura Harrison

Scientific Coordinator

Type 1 Diabetes Immunology (TDI) Helmholtz Diabetes Center (HDC) Heidemannstraße 1 80939 Munich, Building 106