News
ERC Consolidator Grant for Peter Walentek
European Union funds research into the adaptability of tissues
Second Funding Period for NephGen!
The DFG confirmed in their latest press release that the CRC 1453 will receive funding for a second...
Unsere Kollegiatinnen und Kollegiaten im sechsten Förderjahr
Im Folgenden möchten wir Ihnen unsere Kollegiatinnen und Kollegiaten im 6. Förderjahr vorstellen. Sie wurden in einem spezifischen Auswahlverfahren von unserem EKFK-Direktorium in Zusammenarbeit mit dem Evaluierungskomitee ausgesucht.
Dr. Markus Zeisbrich
Klinik für Rheumatologie & Klinische Immunologie
Projekt P04: Podozytenschädigung bei der Lupusnephritis: Pathogenese und neue Therapiestrategien
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with a heterogeneous clinical presentation. Approximately 60% of patients develop nephritis; despite treatment, 10–30% of these patients progress to end-stage kidney disease. Irrespective of improved disease control over the last decades, the rate of complete clinical remissions of lupus nephritis after immuno-suppressive therapy is below 50%.
The failure of immunosuppressive treatment of lupus nephritis might be due to an incomplete understanding of disease pathogenesis. Accumulating evidence indicates that cells of myeloid origin play a significant role in renal damage in SLE patients. In glomeruli of affected patients, increased numbers of infiltrating CD16+ monocytes were observed. Specifically, patrolling monocytes were shown to be key drivers of glomerular disease, in contrast to T or B cells that were dispensable for disease progression. However, it is unknown by which mechanisms these cells contribute to disease.
Myeloid cells, such as monocytes and macrophages, have a strong interrelationship between immunological effector function and cellular metabolism. Their polarization state (pro- or -anti-inflammatory) is driven and can be converted by metabolic checkpoints. Thus, we hypothesize that the regulation of cellular metabolism of kidney-infiltrating monocytes that later differentiate into tissue macrophages shape pathogenic effector functions that might contribute to lupus nephritis.
Mentoren/innen:
1) Prof. Reinhard Voll (Klinik für Rheumatologie und klinische Immunologie)
2) PD Marta Rizzi (Klinik für Rheumatologie und klinische Immunologie)
3) Prof. Cristina Has (Klinik für Dermatologie und Venerologie)