Antibody blockade of CLEC12A delays EAE onset and attenuates disease severity by impairing myeloid cell CNS infiltration and restoring positive immunity.

ABSTRACT: The mechanism of dendritic cells (DCs) recruitment across the blood brain barrier (BBB) during neuroinflammation has been the least explored amongst all leukocytes. For cells of myeloid origin, while integrins function at the level of adhesion, the importance of lectins remains unknown. Here, we identified functions of one C-type lectin receptor, CLEC12A, in facilitating DC binding and transmigration across the BBB in response to CCL2 chemotaxis. To test function of CLEC12A in an animal model of multiple sclerosis (MS), we administered blocking antibody to CLEC12A that significantly ameliorated disease scores in MOG_35-55-induced progressive, as well as PLP_138-151-induced relapsing-remitting experimental autoimmune encephalomyelitis (EAE) mice. The decline in both prog

SUBMITTER: Sagar D 

PROVIDER: S-EPMC5457463 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature