Beneficial role of ILC2s in SCI. (A) Immunofluorescent staining of IL-13^tdt+ ILC2s in the spinal cord 10 d after SCI. Insets show zoomed-in images of representative ILC2s (white arrows, IL-13^tdt+/CD3⁻) or T cells (yellow arrows, IL-13^tdt−/CD3⁺) in the injury site at 10DPI. (B) Time course of ILC2 infiltration into the SCI site measured by flow cytometry (3DPI vs. 10DPI P = 0.016, 3DPI vs. 30DPI P = 0.015, 5DPI vs. 10DPI P = 0.040, 5DPI vs. 30DPI P = 0.039; n = 3, representative of two experiments; one-way ANOVA with Tukey’s multiple comparisons test). (C and D) Single-cell suspensions of SCI sites 10DPI were stimulated and assessed for IL-13 expression (C; P = 0.007; n = 4; Student’s t test). (D) WT and IL-33^−/− mice were injured, and at 10DPI, the injury site was analyzed for ILC2 infiltration (P = 0.741; n = 4 WT and 3 IL-33^−/− mice; Student’s t test). (E) FACS-isolated lung-derived ILC2s (5 × 10³) from WT mice were delivered intracerebroventricularly (i.c.v.) into ST2^−/− animals in 1 µl PBS the day before injury. The control group received 1 µl PBS i.c.v. (P = 0.017; n = 8; repeated measures two-way ANOVA with Šídák’s multiple comparisons test). (F and G) Lesion volume was calculated on injured tissues 30DPI. (F) ILC2-treated mice had smaller lesions (P = 0.040; n = 4; Student’s t test). (G) Representative coronal images of GFAP staining from the center of spinal cord lesions. Error bars represent mean ± SEM; *, P ≤ 0.05; **, P ≤ 0.01.