Today, for most of chronic neuroinflammatory diseases no cure is available. Translating therapeutic concepts and monitoring their efficacy with cutting-edge biomedical technology, will offer unique chances to identify the drivers of inflammation in several diseases, and define innovative ways to stop them. Our aim is to identify cells and mechanisms controlling the chronicity of neuroinflammation and to develop biomarkers and biosignatures identifying the key players to predict the response to therapy for a tailored, individualized therapy.



You are here:

Our main questions are:
How does chronicity change the biosignature of immune cells in neuroinflammation? and is there a tissue memory of inflammation and what are the functional consequences?

Role of B cells and antibody producing cells in chronic neuroinflammation (P17 in TRR130)

We analyze the B cells and plasma cells within the inflamed CNS parenchyma. We want to understand the functional outcome of their presence in the CNS, i.e. B-T interactions and their function in follicular structures and the antibody repertoire. In parallel we will translate our findings and investigate similar to the murine studies the human B cell phenotype and function in chronic neuroinflammation.

Oxidative stress in chronic neuroinflammation

We use an innovative technique based on NAD(P)H-fluorescence lifetime imaging (FLIM), which allows us to specifically detect NAD(P)H-dependent enzymatic functions in living animals and human cells. The NADPHoxidase familiy is mainly responsible for massive reactive oxygen species (ROS) production. We want to understand the mechanisms leading to NOX overactivation and the effect of massive ROS production on the tissue, especially its contributes to neuronal dysfunction correlatively assessed by quantifying neuronal calcium level by means of intravital FRET-FLIM.