AST10.eae2 is a distinct subtype from the previously described AIMS (astrocytes inflamed in MS in chronic active lesions, (129)) as it does not express classical complement components (C1S, C1R); instead, it expresses components and regulators of lectin (MASP1) and the alternative (CFI) complement pathways, which are not triggered by antibody recognition (FigS7B). This evidence concerns the gene C1R and myeloid sarcoma.