Myelin/oligodendrocyte glycoprotein–deficient (MOG-deficient) mice reveal lack of immune tolerance to MOG in wild-type mice
J. Clin. Invest. Cécile Delarasse, et al. 112:544 doi:10.1172/JCI15861 [Go to this article.]

Figure 3
EAE is less severe in MOG^–/– mice. (a) Mean clinical score of EAE induced with rat rMOG in WT (n = 4) and MOG^–/– (n = 4) mice. (b) Mean clinical score of two independent EAE experiments induced with whole myelin in WT (n = 8) and MOG^–/– (n = 13) female mice. MOG^+/+ females developed a more severe EAE than MOG^–/– females (mean maximal clinical score ± SD, 4.4 ± 1.2 in MOG^+/+ vs. 1.5 ± 1.5 in MOG^–/–; P = 0.004, two-tailed Student t test), leading to higher mortality (75% in MOG^+/+ vs. 15% in MOG^–/–; P = 0.006, Fisher’s exact test). Disease onset was also delayed in MOG^–/– mice (mean ± SD, 17.9 ± 6.6 days) as compared with WT mice (13.4 days ± 1.9; P = 0.008, log-rank test). (c) CNS histology of MOG^–/– (left column) and WT mice (right column) at day 20 after induction of EAE with whole myelin. Upper panels (×11): H&E staining showing large infiltrates (arrowheads) in WT mice but no inflammation in MOG^–/– mice. Middle panel (×70): Klüver-Barrera staining for myelin shows no loss of myelin in MOG^–/– mice, but loss of subpial myelin in WT mice. Arrowheads indicate the presence of intramyelinic vacuoles. Lower panel (×70): Immunocytochemistry for CD3 shows the absence of T cell inflammation in MOG^–/– mice, whereas WT mice have large numbers of T cells in inflammatory infiltrates.