Inhibitors for Selectins
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Extravasation of leukocytes into the targeted tissue is a desired process during inflammation and homing. In contrast, in acute inflammatory diseases with excessive immune response and autoimmune diseases, it comes to an uncontrolled migration of leukocytes into the affected tissue. In the case of autoimmune diseases (e.g. Crohn's disease or rheumatiod arthritis) endogenous structures are recognized by the immune system as foreign. In acute inflammatory or chronic inflammatory diseases with excessive immune response these pathologically increase in migration of leukocytes is due to an excess of pathogens / noxious substances, such as Bacteria (pneumonia) and viruses (myocarditis) or toxins (chronic obstructive pulmonary disease, COPD) and uncontrolled enzyme reactions (pancreatitis). The reason is that the inflammation-causing toxicants exceed the bandwidth of the regulation of the immune response with the result that the excessive emigration of leukocytes not only eliminate the noxious substances, but leads to additional tissue damage.
The members of the selectin family (L-, P- and E-selectin) mediate the capturing, rolling and slow rolling of the leukocytes. Therefore, they are good candidates to engage in the process of leukocyte extravasation.
Characterisation of known and design of novel selectin inhibitors which reduce leukocyte adhesion to develope new therapeutics.
Examples for different inhibitors
- Polymers, e.g. polyglycerol sulfate
- Functionalized nanoparticles
- Small molecules, e.g. Efomycin M
Rolling cells with and without inhibitor