We employed a fusion between αDCIR2 antibodies and the highly encephalitogenic peptide 139-151 of myelin-derived proteolipid protein (PLP<sub>139-151</sub>), to target CD11c <sup>+</sup>CD8<sup>-</sup> DCs with a DEC-205-DCIR2<sup>+</sup> phenotype in vivo, and to substantially improve clinical symptoms in the PLP<sub>139-151</sub>-induced model of experimental autoimmune encephalomyelitis (EAE).
LysM-EGFP//CD11c-EYFP mice appear as a powerful tool to differentiate moDCs from macrophages and to study the dynamics of immune cell maturation and phenotypic evolution in EAE.
Using flow cytometry analysis, we observed an increase of the percentage of CD11c-GFP<sup>+</sup> cells in brain parenchyma in the course of EAE which is most likely due to an up-regulation of CD11c of resident microglial cells since levels of gfp gDNA did not increase.
In this study, we demonstrated that subcutaneously administered myelin basic protein (MBP)-pulsed CD11c+ bone marrow-derived dendritic cells (BMDC) were as effective at inducing EAE as subcutaneously administered MBP plus CFA.