MPM 5 - Overview
Many diseases are the result of failures or dysfunction in our body’s defense mechanisms. This module will develop a deep and mechanistic understanding of our immune system. The module will examine primary immunodeficiencies, autoimmune and autoinflammatory diseases, allergies, and emerging concepts in immune regulation. Paradigmatic diseases will be used to illustrate what can go wrong in our immune system, disease diagnosis, and therapeutic strategies.
MPM 5 - Details
Module 5 will provide students with a basic introduction to the key principles of our immune system, expand on inborn errors of immunity, autoimmune and autoinflammatory diseases, allergies, and emerging concepts in immune regulation. Paradigmatic immune diseases will be discussed to illustrate the precise mechanisms and contribution of our immune system, and how precision medicine-based approaches can be exploited for diagnosis, disease prevention and therapeutic purposes.
Module 5 is structured in three parts, and in each part there will be lectures and interactive Q&A and discussion sessions with lecturers. The three parts of Module 5 are complemented with seminars, in which emerging concepts related to molecular precision medicine approaches in immunity, inflammation and infection will be discussed.
The aim of the first part of MPM5 is to provide students with an overview of basic concepts and key players of the immune system, including developmental aspects. Subsequently, innate host defense mechanisms to bacterial infections and examples of their pathological dysregulation will be described at the molecular level. Further, molecular, cellular and clinical aspects of inborn errors of the immune system will be discussed.
The aim of the second part is to discuss the molecular and cellular basis of autoimmunity, using rheumatoid arthritis, and disorders involving the skin, the gastrointestinal tract and the CNS as examples for precision medicine approaches. Moreover, the development, diagnosis and therapy of allergic diseases will be discussed. Furthermore, the implication of metabolism in immune-mediated diseases and their therapies will be discussed.
In the third part, we will discuss examples of how the immune system can be harnessed for preventative and therapeutic approaches. Novel cell-based therapies (CAR-T cells) will be presented. We will provide an introduction to prophylactic medicine, in particular vaccination strategies in the context of preventing cancer and with a nod to the current Coronavirus pandemic.
Teaching faculty include basic research scientists from the Max Perutz Labs, the Medical University of Vienna, and the Ludwig Boltzmann Institute for Rare and Undiagnosed Diseases, as well as clinicians from the Medical University of Vienna and St. Anna Children’s Cancer Research Institute.
Module coordinators
Wilfried Ellmeier
Wilfried Ellmeier is a Professor of Immunobiology at the Medical University of Vienna. His research investigates the molecular mechanisms that regulate the development and function of T-lymphocytes (T-cells) in the immune system. Dysregulated T-cells are often the cause of human disease. Wilfried’s research aims to provide important and medically-relevant insights into the regulation of T-cell mediated immunity.
Georg Stary
Georg Stary's scientific focus is on gaining a better understanding of the immune system of the skin and mucous membranes and investigating how this can be used to prevent or treat diseases. Already during his medical studies, he researched the contribution of various immune cells in inflammatory skin diseases and how they are influenced by different stimuli. To this end, he expanded his knowledge of immunodermatology and technological skills during a research stay of several months at the Department of Dermatology at Harvard University in Boston, Massachusetts. "This early exposure to dermatological research was certainly a key factor in my subsequent decision to become a dermatologist and complete my specialist training at the Medical University of Vienna," explains Georg Stary.