Harnessing GPR17 Biology for Treating Demyelinating Disease.

摘要

The overarching hypothesis of this project was that GPR17 signaling results in blockade of remyelination in neuroinflammatory lesions. We thus predicted that GPR17 could serve as an important target for promoting remyelination in these lesions. The specific aims of this study were: (1) To delineate the role of GPR17 in murine models of demyelinating diseases; and (2) To test the therapeutic potential for GPR17 agonists and antagonists in two models of multiple sclerosis. Our studies demonstrate that GPR17-deficient mice developed less severe disease and recovered faster from paralysis. Moreover, these mice showed reduced CNS-targeted pathogenic immune responses. These results provide us a strong basis to pursue drugbased treatment for this disease in the future.