Their FcγRI-expression was greatly increased by IFN-γ [69] and they were also activated by antigen-IgG complexes binding to their Fc-γRIs (IgG2a only) and Fc-γRIIIs [68], which resulted in MIP-1α-release and neuronal apoptosis, and which has been implicated in a wide range of neurological diseases [70]. This evidence concerns the gene CCL3 and nervous system disorder.