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. 2019 Aug 12;129(9):3754–3769. doi: 10.1172/JCI128010

Figure 4. FcγRI mediates IgG-IC–induced acute joint nocifensive behaviors in mice.

Figure 4

(AC) Comparison of basal mechanical sensitivity to ankle press (A) and to plantar stimulation with von Frey filaments (B), and basal thermal sensitivity to plantar application of radiant heat (C), between Fcgr1+/+ (n = 9 mice) and global Fcgr1–/– mice (n = 12 mice). P > 0.05; unpaired Student’s t test or 2-way ANOVA for repeated measures followed by Bonferroni’s post hoc test. (DF) Global Fcgr1–/– mice (n = 12 mice) exhibited a higher mechanical threshold in the ankle (D) and lower paw withdrawal frequency (PWF) to 0.07 (E) and 0.4 g force (F) applied to the hind paw following i.a. injection of IgG-IC (100 μg/mL; 10 μL) compared with Fcgr1+/+ control littermates (n = 9 mice). *P < 0.05 vs. Fcgr1+/+ controls, #P < 0.05 vs. before injection; 2-way ANOVA for repeated measures followed by Bonferroni’s post hoc test. (G and H) Depletion of synovial macrophages with liposomal clodronate (5 mg/mL; 6 μL) had no significant effects on mechanical hyperalgesia in the ankle (G) or hind paw (H) in mice upon injection of IgG-IC, compared with liposomal control (Veh). n = 10 mice per group; P > 0.05; 2-way ANOVA for repeated measures followed by Bonferroni’s post hoc test. (IL) No significant differences were seen in IgG-IC–induced mechanical hyperalgesia in the ankle and hind paw in mice lacking T cells (Rag1–/–) or mast cells (c-KitW-sh/W-sh) compared with WT controls. n = 10–11 mice per group; P > 0.05; 2-way ANOVA for repeated measures followed by Bonferroni’s post hoc test.