Anti-glycan Ab-mediated inhibition of axon regeneration was dependent on the expression of activating FcγRs.

<p>Behavioral studies (Pinprick test) showing the effects of GD1a/GT1b-2b mAb and sham Abs on sensory functional recovery after nerve injury in WT control mice (A), or <i>Fcer1g</i>-null mice (B). *<i>p</i> < 0.01 (Student’s <i>t</i> test). Quantitative electrophysiology showing the CMAP amplitudes of GD1a/GT1b-2b mAb- or sham Ab-treated WT or <i>Fcer1g</i>-null mice (C). Representative micrographs from sciatic nerve segments distal to the crush site in GD1a/GT1b-2b mAb-treated WT (D) or <i>Fcer1g</i>-null (E) mice. Morphometric analysis (MF counts) in sciatic (F) or tibial (G) nerves from WT or <i>Fcer1g</i>-null mice treated with sham Ab or GD1a/GT1b-2b mAb. *<i>p</i> < 0.001 (Two-way ANOVA, Tukey’s multiple comparisons test). N = 10–12 per group. Error bars, s.e.m. Scale bar, 10 µm. WT = wild type; NS = not significant; MF = myelinated nerve fibers.