Welcome to the Institute of Cardiovascular Immunology!
Our main goal is the achievement of new insights into the intricate mechanisms of viral immunorecognition and the development of autoimmune diseases. In a field where solutions are rather rare to find, this gain of knowledge enables us to contribute to the development of new innovative therapeutics.
Recent publications, conferences, new members and more…
Our research focuses mainly on two main topics dealing with the analysis of molecular mechanismisms leading to autoimmune diseases (ADs) and the molecular mechanisms during viral recognition.
In both processes cytoplasmic RNA sensors, namely RIG-I like receptors (RLRs), play a crucial role. Their role is more obvious during virus recognition since RLRs distinguish between viral RNAs and self-RNAs and trigger type I interferons (type I IFNs) as a defense mechanism. But it has also been found, that mutations in RLR lead to the development of several autoimmune diseases.
Retinoic Acid Inducible Gene I (RIG-I) and Melanoma Differentiation Associated Gene 5 (MDA5) are two key molecules we are investigating among the RLRs .
Currently more than 100 different autoimmune diseases (ADs) are known, affecting 10% of the european and 8% of the american human population. The reasons for developing a AD are multifactorial and include genetic predisposition, environmental factors and the individual way of living.
Amongst the genetically caused ADs is a group of disorders having an abnormal upregulation of type I IFN in common and are therefore called interferonopathies. They comprise diseases like systemic lupus erythematosus (SLE), Singleton-Merten Syndrom (SMS), Aicardi-Goutieres Syndrom (AGS) und type 1 diabetes (T1D).
Two key molecules in interferonopathies are RIG-I and MDA5. Mutations in both could be connected to the development of ADs and interferonopathies. RIG-I and MDA5 are intracellular receptors of viral nucleic acids leading to the initiation of an immune reaction and the production of pro-inflammatory interferons. Misregulations within this process can lead to an over reacting immune response yielding in ADs and interferonopathies.
Virus destruction by a cell needs specific receptors, which recognize viral-specific components and initiate an appropriate immune response. Amongst these components are for example double-stranded RNA molecules (dsRNA) which do not appear in normal and healthy cells and are therefore categorized as foreign material.
The differentiation is done by specific receptors like RIG-I and MDA5. Although both molecules spot dsRNA, it was shown that they still comprise virus-specificity. It was proven that RIG-I and MDA5 are crucial for effective destruction of these viruses during infection.
Upon viral recognition by RIG-I or MDA5 a signaling cascade is initiated resulting in the production of pro-inflammatory cytokines and chemokines. The activation of these signaling cascades has to be tightly regulated to initiate an effective immune response without yielding in a overproduction of cytokines which would result in a deadly so called cytokine storm.
We proudly present our latest publiations and reviews
