Increased parenchymal synthesis of C1q precedes blood–brain barrier dysfunction[34], C1q can contribute to the endothelial expression of Vcam1[36], C1q binding to target cell-bound NMO-IgG can trigger antibody-dependent and/or complement mediated cytotoxicity[37,38], and the local activation of complement can trigger neutrophil recruitment[39]. Here, VCAM1 is linked to neuromyelitis optica.