Research target
Scientists at the Franz Volhard Clinic for Cardiovascular Diseases of the Charité – University Medicine Berlin/HELIOS-Klinikum and the Max Delbrück Centre for Molecular Medicine (MDC) Berlin-Buch have discovered that a specific surface receptor, NB1, mediates the expression of an antigen on the surface of certain white blood cells, where the immune system recognises and binds it.
This reaction initiates the blood vessel inflammation process that characteriaes vasculitis, making NB1 a potential drug target for this autoimmune disease.
Autoimmune vasculitis is a broad term encompassing a group of disorders characterised by blood vessel inflammation. It is triggered by antibodies formed by the immune system which are no longer able to distinguish between “self” and “non-self”. The antibodies target the most common white blood cells, the neutrophil granulocytes, or more precisely an enzyme that is normally found in the cell plasma of these blood cells, proteinase 3 (PR3).
The binding of antibodies to PR3 localised on the cell membrane activates the white blood cells, which trigger the inflammation processes in the blood vessels. The resulting inflammation can affect any and all organs and become life-threatening.
Before this study it was not known how the PR3 is presented on the membrane surface of the blood cells. The scientists showed the membrane anchor protein NB1 is necessary for PR3 to be expressed on the cell surface.
The researchers say NB1 inhibition could prevent PR3 from being expressed on the blood cell surfaces, thus controlling, or even preventing, the vasculitis.
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