Table 1. Adoptive transfer of cells from PLP139–151 16-mer treated mice.
Transfer | Donor | No. EAE | Mean Group Score ±SEMa | Mean EAE Score ±SEMb | Mean Day of Onset ±SEM |
B220+ cells | Oligomer treated mice | 3/5 | 1.4±0.6 | 2.3±0.3 | 13.3±1.4 |
Untreated mice | 4/5 | 2.8±0.8 | 3.5±0.5 | 12.2±0.6 | |
EAE Control – No transfer | 5/5 | 3.0±0.3 | 3.0±0.3 | 12.2±1.0 | |
CD4+CD25+ | Oligomer treated mice | 3/4 | 1.7±0.6 | 2.3±0.3 | 8.3±0.3 |
CD4+CD25− | Oligomer treated mice | 4/4 | 2.5±0.3 | 2.5±0.3 | 13.5±2.6 |
EAE Control – No transfer | 3/4 | 3.0±1.2 | 4.0±1.0 | 13.7±1.2 | |
Spleen cells | Oligomer treated mice | 3/4 | 2.5±1.2 | 3.3±1.2 | 10.0±1.0 |
CFA primed mice | 4/4 | 4.2±0.7 | 4.2±0.7 | 11.7±0.7 |
Subpopulations of B220+, CD4+CD25+ and CD4+CD25− cells were purified from CFA primed mice and oligomer treated and untreated SJL/J mice. Cell separation was performed by immunomagnetic sorting. 5×106 total spleen cells or 5×106 cells from each subpopulation were resuspended in PBS 1% FCS and intravenously injected into recipient mice, one day before the EAE induction. The effect of adoptive cell transfer to modulate the evolution of EAE was assessed. Animals were monitored daily for development of EAE.
Mean ± SEM of maximum clinical score of EAE from all animals in the group.
Mean ± SEM of maximum clinical score from animals exhibiting EAE within a group.