The objective is to elucidate the pathogenesis and pathophysiology of glomerular diseases and vasculitides with the ultimate goal to develop effective modalities to treat inflammatory processes in the kidney and in vessel walls. The processes leading to chronic damage and severe functional loss are studied with the purpose to design effective prevention of the development of terminal renal failure.
- Future themes:
We expect to continue our work on the involvement of complement activation in early stages of glomerulonephritis, and to develop mouse models of renal inflammation, allowing the analysis of genetically modified animals. We will further explore the recently described Mannan Binding Lectin (MBL) pathway of complement activation, and we will expand the research on IgA receptors involved in the pathogenesis of IgA nephropathy.
- Research goals:
* Develop small peptide inhibitors, capable of efficiently inhibiting the first step of complement activation
* Investigate the involvement of C1q-anti-C1q complexes in the development of experimental glomerulonephritis
* Define the relationship between the complement system and induction and clearance of apoptotic cells
* Investigate the interaction between IgA and cell surface receptors, either known (CD89, pIgR, lectins) or to be identified, involved in IgA biology. |
