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. 2003 May 5;197(9):1073–1081. doi: 10.1084/jem.20021603

Table II.

EAE Induced in 2D2 TCR Transgenic Mice and Negative Control Littermates

Clinical EAE
Histological EAE
Treatmenta Incidence Mortality Mean day of onsetb Mean maximal scorec Incidenced Mean number of focie
MOG35–55 + PT Tg 9/10 (90%) 4/10 (40%) 11.9 ± 1.2 4.0 ± 0.3 8/10 (80%) 170.9 ± 38.3
NT 9/11 (82%) 0/11 (0%) 14.5 ± 2.2 2.6 ± 0.4 8/10 (80%) 78.9 ± 24.9
PT alone Tg 9/23 (39%) 3/23 (13%) 14.1 ± 2.1 3.8 ± 0.3 9/16 (56%) 39.3 ± 11.4
NT 0/6 (0%) 0/6 (0%) NA NA 1/5 (20%) 5.5 ± 4.1
MOG35–55 100 μg Tg 0/9 (0%) 0/9 (0%) NA NA 0/9 (0%) 2.4 ± 0.9
NT 0/9 (0%) 0/9 (0%) NA NA 1/5 (20%) 5.0 ± 2.9
MOG35–55 10 μg Tg 0/9 (0%) 0/9 (0%) NA NA 0/9 (0%) 2.3 ± 1.0
NT 1/9 (11%) 0/9 (0%) 23 ± 0 2 ± 0 4/10 (40%) 16.9 ± 7.2
a

2D2 TCR transgenic (Tg) and nontransgenic (NT) littermates were immunized by various regimens including MOG35–55 peptide in CFA and pertussis toxin (PT), PT alone, or MOG peptide alone in CFA. The animals were then monitored for signs of EAE.

b

Data are presented as mean ± SE.

c

Data are presented as mean maximal clinical scores for the animals showing clinical disease.

d

Mice with >10 lesions in brain and spinal cord were considered positive.

e

Data are presented as mean number of meningeal and parenchymal inflammatory lesions in brain and spinal cord.