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).
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.
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.