Fig. 4: The anti-CD20 monoclonal antibody reverses CRMP5 autoimmunity-induced mechanical hypersensitivity and hyperexcitability.
From: Anti-CV2/CRMP5 autoantibodies as drivers of sensory neuron excitability and pain in rats
Male rats were immunized against CRMP5 and developed stable mechanical hypersensitivity up to day 86 after the first intramuscular injection. A Graph showing the paw withdrawal threshold of rats over time. Black arrows show the three plasmid injections necessary for the induction of the model. Anti-CD20 injection (4 mg/kg, i.p.) is indicated at days 56 and 63 by an antibody symbol. Control + Anti-CD20 n = 6, CRMP5 autoimmunity + Vehicle n = 8, CRMP5 autoimmunity + anti-CD20 n = 6, *p < 0.05 two-way ANOVA. B Bar graph with scatter plot showing the area under the curve for each individual from the indicated treatment groups. CRMP5 autoimmunity + Vehicle n = 8, CRMP5 autoimmunity + anti-CD20 n = 6. *p < 0.05, two-tailed, Mann–Whitney test. C Representative recordings of evoked action potentials recorded from rat small-diameter DRG neurons cultured from the indicated treatment groups in response to depolarizing current injection of 30, 60, and 90 pA. D Quantification of the number of current-evoked action potentials in response to 0–100 pA injected current. CRMP5 autoimmunity increased action potential firing compared to control DRG neurons. Anti-CD20 reversed this phenotype back to the level of control sensory neurons. *p < 0.05, multiple Mann–Whitney tests. Control + Anti-CD20 n = 9 cells, CRMP5 autoimmunity + Vehicle n = 9 cells, CRMP5 autoimmunity + anti-CD20 n = 8 cells obtained from at least three rats. All data are shown with error bars that indicate mean ± SEM. See Supplementary Data 1 for additional statistical details. Source data are provided as a Source Data file.
