Table 2.

Development of aEAE in SJL/J Mice Treated With Repeated Injections of Anti–E-Selectin and/or Anti–P-Selectin MoAbs

TreatmentNo. of AnimalsNo. of Animals Developing Clinical DiseaseMean Day of Onset of Clinical Disease*No. of Animals With Detectable Infiltrates in CNS
⊘ 15 11 13.8 ± 4.5 15 
PBS 11 13.8 ± 1.9 11 
IgG 14.0 ± 0.7 
RB40 (anti–P-selectin) 15.3 ± 3.2 
UZ4 (anti–E-selectin) 15.3 ± 5.3 
RB40 + UZ4 13.5 ± 0.5 
TreatmentNo. of AnimalsNo. of Animals Developing Clinical DiseaseMean Day of Onset of Clinical Disease*No. of Animals With Detectable Infiltrates in CNS
⊘ 15 11 13.8 ± 4.5 15 
PBS 11 13.8 ± 1.9 11 
IgG 14.0 ± 0.7 
RB40 (anti–P-selectin) 15.3 ± 3.2 
UZ4 (anti–E-selectin) 15.3 ± 5.3 
RB40 + UZ4 13.5 ± 0.5 
*

Only animals developing clinical disease were taken into account.

Animals were sacrificed 4 days after onset of clinical disease for histopathological analysis of the CNS tissue, making statistical analysis of clinical severity of the disease at the same time impossible. Although not all animals developed a clinical disease, they all showed inflammatory cuff formation in their spinal cords and brains. No significant differences were observed in number and size of inflammatory cuffs when comparing the different treatment groups or clinically diseased versus nondiseased aEAE animals.

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