Fig. 10

Diagrammatic representation of the possible mechanisms of action for the anti-CD1d treatment in synucleinopathy models. Extracellular α-syn aggregates targeting TLR’s activate microglia and astrocytes that might work as APCs in the CNS, in turn producing cytokines and chemokines (e.g.: CCL4) that attract migration of T cells and NKTs. Since neurotoxicity might occur when presenting lipid antigens by APCs CD1d- activate NKT cells, blocking the APC-NKT interaction with an anti-CD1d antibody reduces neuroinflammation and neurodegeneration by abrogating the production of toxic cytokines