FIGURE 6. Disease protection requires both CD56^bright and CD56^dim subpopulations.

(A) PBMC of control and MS subjects were treated with IL-2 C as described for Fig. 5. CD56⁺subsets were sorted. CD56^bright and CD56^dim cells differentially expressed CCR7, CD117, IL-18R and CX3CR1 (right panel). Clinical scores of EAE in RAG1^−/−γc^−/− mice after co-transferring CD56^bright or CD56^dim subsets (2.5–5 ×10⁵) with PLP-reactive T cell lines (1–2 ×10⁶) raised from the same MS patients whose NK cells are used in the experiments (left panel). P is greater than 0.05 at all time points for comparisons among the group that received T cells only and groups that received T cells together with CD56^bright or CD56^dim cells. P values varied between 0.036–0.078 at all time points for comparisons among the groups that received T cells together with unfractionated CD56⁺ cells and groups that received T cells together with CD56^bright or CD56^dim cells. P<0.01 at all time points for comparisons between the groups that received T cells only and groups that received T cells together with unfractioned CD56⁺ cells. P values for clinical scores were evaluated by Mann-Whitney U test, n=15–20/group. The expression of differential markers was evaluated by Student’s t-test, *p<0.05, **p<0.01; n=6 MS subjects. (B) Proliferation of transferred CD56⁺ cells and their subsets was quantified by BrdU. PBMC from 15 donors and 15 recipient animals in each group were studied.