Fig. 5

CCL2 plays an important role during recruitment of γδ T cells to lesions. a BMS score of WT and CCL2^−/− mice at different time points after spinal cord injury (SCI) (n = 8 mice/per group). b Max contact area of WT and CCL2^−/− mice at 6 weeks after SCI (n = 8 mice/per group). c Regularity index of WT and CCL2^−/− mice at 6 weeks after SCI (n = 8 mice/per group). d Cadence of WT and CCL2^−/− mice at 6 weeks after SCI (n = 8 mice/per group). e Motor-evoked potential (MEP) recordings from WT and CCL2^−/− mice at 6 weeks post-surgery (n = 8 mice/per group). f Spinal sections from WT and CCL2^−/− mice after 1 day post-SCI were immunostained with anti-TCRγδ (green, a maker for γδ T cell) and the corresponding static histogram of percent of γδ T cell (γδ T cells/total cells) (n = 6 mice/per group). g Survival of motor neurons immunostained with Nissl staining in cross-section of spinal cord lesion epicenter at 6 weeks after SCI (n = 6 mice/per group). **P < 0.01; ***P < 0.001; ****P < 0.0001