Fcγ Receptor-Mediated Inflammation Inhibits Axon Regeneration
Figure 4
Anti-glycan Ab-mediated inhibition of axon regeneration was dependent on the expression of activating FcγRs.
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 Fcer1g-null mice (B). *p < 0.01 (Student’s t test). Quantitative electrophysiology showing the CMAP amplitudes of GD1a/GT1b-2b mAb- or sham Ab-treated WT or Fcer1g-null mice (C). Representative micrographs from sciatic nerve segments distal to the crush site in GD1a/GT1b-2b mAb-treated WT (D) or Fcer1g-null (E) mice. Morphometric analysis (MF counts) in sciatic (F) or tibial (G) nerves from WT or Fcer1g-null mice treated with sham Ab or GD1a/GT1b-2b mAb. *p < 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.