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Table 1 Comparison of MOG-IgG with AQP4-IgG lesions in mouse brain

From: Neuromyelitis optica MOG-IgG causes reversible lesions in mouse brain

Characteristic MOG-IgG AQP4-IgG
Target cell Oligodendrocyte (myelin) Astrocyte (foot process)
Lesion onset Within hours of exposure to MOG-IgG Within hours of exposure to AQP4-IgG
Effect on astrocytes No major effect (normal AQP4 and GFAP) Astrocyte death (loss of AQP4 and GFAP)
Effect on neurons No major effect Neuronal death (loss of NeuN, FJ-C staining[5])
Effect on oligodendrocytes Change in myelin (loss of LFB) Loss of myelin (loss of LFB)
Effect on axons Myelin (transient change in MBP) Permanent loss of myelin
  Intact axons (normal nfil) Axonal degeneration (β-APP expression[5])
  Node of Ranvier (transient change in casp and ankG)  
Inflammatory cell infiltration No Yes
Complement activation Slight (in white matter tracts) Marked (perivascular)
  Not required for lesion to develop Essential for lesion to develop
Recovery Yes, within 2 weeks No, pan-necrosis followed by glial scarring
  1. β-APP, beta amyloid precursor protein; FJ-C, fluorojade C; GFAP, glial fibrillary acidic protein; LFB, Luxol fast blue; MBP, myelin basic protein; NeuN, neuronal nuclear marker; nfil, neurofilament.