Our research projects are a compli(e)ment to the eye.
We investigate the molecular role of the complement system, part of the innate immune response, in eye diseases.
An EU wide project to investigate the Factor H related protein family
Diana Pauly - project coordinator
Veronika Ehinger - project management
Pratiti Banerjee - scientist
Millions of people in the European Union suffer from diseases associated with dysregulation of the complement system. This can be bacterial infections like invasive meningococcal disease, chronic inflammation of the kidney or, as in 15 million elderly european residents, age-related macular degeneration resulting in impaired vision.
SciFiMed will investigate the pathophysiology of the FH-protein family, to enable the development of personalized, radically new on-time diagnostics, which allow improved patient stratification for prospective cohort studies to understand complement-associated diseases.
SciFiMed work packages are divided between 8 european academic and industrial partners.
In our lab in Marburg, we manage and coordinate the project and focus on investigating structural and functional interaction partners of the Factor H related protein family using phage-display library and mass spectrometry.
For detailed information see www.scifimed.eu.
COMPLEMENT IN RETINAL PIGMENT EPITHELIUM CELLS
The retinal pigment epithelium (RPE) is one of the retinal layers and forms the outer blood-retinal barrier to establish the immune-privileged structure of the retina. With a variety of important functions the RPE helps to maintain our eyesight. Under pathological conditions the RPE is able to undergo epithelial mesenchymal transition (EMT) and loses its mature form, unable to preserve its vital role in the retina. Our goal is to characterize the maturation of the RPE and analyze the role of the complement system in this process, using the immortalized human cell line ARPE-19 as well as RPE cells derived from human induced pluripotent stem (iPS) cells.
THE ROLE OF COMPLEMENT IN RETINAL DEGENERATION IN NMOSD
Neuromyelitis optica spectrum disorder is an autoimmune disease caused by anti-Aquaporin4 IgG. Common knowledge suggests primary disease activity along the optic nerve and spinal cord. Recent evidence however indicates retinal degeneration in NMOSD patients without occurence of optic neuritis. Our goal is to identify the role of complement in inner-blood-retinal barrier disruption and thereby investigate how complement contributes to autoantibody transmigration.