Ac-4,4-diF-GlcNAc 16 attenuates EAE. (A) Average daily
EAE clinical score of mice treated daily with 25 mg/kg Ac-4,4-diF-GlcNAc 16 or saline vehicle (N = 8) with treatment
shown by arrows; mice are analyzed in parts C to G. (B) Sum of scores
displaying individual burden of disease. (C) Brightfield images of
F4/80 and CD45 and immunofluorescence of CD45 and laminin in vehicle-
or Ac-4,4-diF-GlcNAc (16)-treated mice (scale bar 50
μm). (D) Flow cytometry of the spinal cord showing Ac-4,4-diF-GlcNAc 16 treatment reduces %CD3+ T cells and %CD45HiCD11b+
monocytes/macrophages (and median fluorescence intensity). (E) Average
perivascular cuffs per spinal cord per mouse in treated and vehicle-treated
EAE mice. (F) Immunohistochemistry of perivascular cuffs next to the
Imaris-processed image (bar = 50 μm). (G) Number of CD45+ cells
within 100 μm of perivascular cuffs, quantified by Imaris. (H)
Average daily EAE clinical score of mice treated with 25 mg/kg Ac-4,4-diF-GlcNAc
or vehicle from peak clinical severity (N = 8). (I)
Average daily EAE clinical score of EAE mice treated with 50 mg/kg
Ac-4,4-diF-GlcNAc 16, Ac-4-F-GlcNAc 3, or
vehicle from preonset (N = 10); arrows indicate daily
injections. *P < 0.05, **P <
0.01, ****P < 0.0001. EAE scores (parts A, H,
and I) were analyzed by two-way repeated-measures ANOVA with Sidak’s post hoc test versus vehicle; mean ± s.e.m. Parts B,
D, E, and G were analyzed by two-tailed unpaired t test; mean ± s.d.