However, if T cells were not activated at all in the CNS – as exemplified by MOG-specific T cells –, recruited macrophages/activated microglial cells in extremely low numbers, and did not compensate for low IFN-γ production levels by high parenchymal cell numbers, astrocyte-destructive lesions in the presence of NMO-IgG and complement were not formed despite inflammation-induced blood–brain barrier leakage. This evidence concerns the gene MOG and neuromyelitis optica.