Diabetology (AG Seißler)

Research Group Xenotransplantation and Cell Therapy

Type 1 diabetes (T1D) is caused by complete destruction of insulin-producing pancreatic islet cell leading to life-long dependence on daily insulin injections. It has been shown that transplantation of pancreas or islolated islets can cure the disease. However, this aproach is limted by the requirement of large numbers of high quality islets and the shortage of organ donors. Porcine islets are a promising alternative cell source, but translation of pig islet transplantation into clinical practice is hampered by the strong xenoreactive rejection.

Previous work

Our research group has shown for the first time that it is possible to cure type 1 diabetes by the transplantation of porcine islets with specific genetic modifications.

Pig islets overeexpressing the immunomodulatory molecules LEA29Y were protected form human immune cell attacks in NOD-scid-IL2γnull (NSG) mice after transfer of human PBMCs and in NSG mice carrying a stable human immune system (hCD34+ cell transfer model).

Aims of research

To identify the best transgene-knock-out combinations needed to achieve long-term acceptance against grafted porcine islets with minimized systemic immunosuppression
To identify novel immunomodulatory therapies that induce active tolerance against porcine islets and can be applied in humans
To provide preclinical data to advance xenotransplantation to a position to perform clinical pilot studies in patients with T1D

Research Group Type 2 Diabetes

Our mission is to improve the health of individuals with prediabetes and diabetes by the identification of specific diabetes subtypes and the establishment of novel individualized therapies.

Previous work

In the population-based KORA-study and the prediction, prevention and subclassification of diabetes study (PPS-Diab) we identified specific patterns of serum biomarkers, metabolites and genetic markers associated with progression to type 2 diabetes and cardiovascular complications.

We characterised the clinical and metabolic profiles of persons at increased risk for diabetes and we have identified a subgroup of high risk patients who display no signs of metabolic syndrome.

Aims of research

To analyse the pathophysiological mechanisms involved in the development of different subtypes of type 2 diabetes
To characterise the link between genetic, metabolic and environmental factors leading to deterioration of beta-cell function
To screen for predictive biomarkers of prediabetes using novel omic-technologies
To test new interventions strategies

Team

Prof. Dr. med. Jochen Seißler Leiter der Diabeteologie Jochen.Seissler@med.uni-muenchen.de

PD Dr. med. Cornelia Then Cornelia.Then@med.uni-muenchen.de

Dr.med.vet. Lelia Wolf van Bürck Lelia.van_Buerck@med.uni-muenchen.de

Dr. Mohsen Honarpisheh Mohsen.Honarpisheh@med.uni-muenchen.de

Monika Pehl Monika. Pehl@med.uni-muenchen.de

Yichen Zhang Yichen.Zhang@med.uni-muenchen.de

Diabetology (AG Seißler)

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