Fig. 2.

The immune neuroprotection evoked by spinal cord contusion is transferable in SPD rats. A, Rats were subjected to spinal cord contusion. One week later their spleens were excised and incubated in vitro with PECs as antigen-presenting cells and with MBP. After 3 d the activated spleen cells were collected, washed, and counted. The resuspended cell population (4.5 × 10⁷) or PBS was injected into rats newly subjected to spinal contusion (n = 5 for each group). In a separate experiment (B), similarly prepared splenocytes from spinally contused rats activated ex vivo with MBP (Contused-MBP; n = 4) or OVA (Contused-OVA; n = 5), or splenocytes prepared from sham-operated animals activated with MBP (Naive-MBP; n = 5), were transferred to newly contused rats. A group of newly contused rats injected with PBS (n = 5) was also included. No effect was seen with splenocytes from contused rats incubated in vitrowith OVA. Similarly prepared splenocytes, withdrawn from rats 14 d (C) or 3 d (D) after spinal contusion, were activated with irradiated thymocytes in the presence of MBP. After 3 d in vitro the activated spleen cells were collected, washed, and counted. The resuspended cells were injected into six rats newly subjected to spinal contusion (4.5 × 10⁷ cells per rat). In each experiment (C, D), five rats that were subjected to spinal contusion and injected with the vehicle (PBS) served as control. E, Transfer of splenocytes withdrawn 14 d after spinal cord contusion and injected with no previousex vivo activation into five rats newly subjected to spinal cord contusion. Five rats that were subjected to spinal contusion and injected with the vehicle (PBS) served as control. Behavioral outcome was evaluated according to a double-blind protocol, using a locomotor test with scores ranging from 0 to 21 (see Materials and Methods). Results are expressed as the mean ± SE at each time point tested. Repeated-measures ANOVA revealed significant effect (p < 0.05) in A–C and no effect inD and E.