Fig. 5.

Induction and characterization of EAE in Crry^−/− mice. (A) Clinical disease score for EAE, showing earlier onset and increased disease severity in Crry^−/− mice (n = 6) compared with WT (n = 4). All animals were killed by day 21. Values are expressed as mean ± SD. Error bars are for n, number of animals. *P < 0.05 determined by Mann–Whitney U nonparametric test. (B–M) Inflammation and myelin loss were assessed by H&E staining (B–D), Iba-1 immunostaining of macrophages (E–G), and IL-1β immunostaining (H–J) and LFB staining (K–M) of myelin in WT (B, E, H, and K) and Crry^−/− (C, F, I, and L) EAE spinal cords. Perivascular infiltration, Iba-1–positive microglia/macrophages, IL-1β deposition, and demyelination were evident in Crry^−/− spinal cords (arrows in C). Arrowheads in K and L indicate a blood vessel. (Scale bars: 100 μm.) Quantification of perivascular infiltration (D), Iba-1 staining (G), IL-1β deposition (J), and perivascular LFB staining (M) in Crry^−/− mice compared with WT. Values are expressed as mean ± SD. Error bars are for n, number of animals. *P < 0.05 in D and M; *P < 0.01 in G and J; determined by two-tailed Student's t test.