Fig. 5: Alleviation of EAE symptoms in hCXCR2 knock-in mice by abN48-2-IgG1.
a Schematic illustration of abN48-2-IgG1 treatment in an EAE mouse model. b Result of PK study of abN48-2-IgG1 in hCXCR2 knock-in mice (n = 4 mice per group). c, d EAE score and body weight of hCXCR2 knock-in mice during abN48-2-IgG1 treatment (n = 4 mice per group). e Comparison of neutrophils in peripheral blood of experimental mice. One blood sample was collected from each mouse in the indicated groups: “Naive” represents the group (n = 4 mice) without EAE stimulation; “isotype Fc” represents the group (n = 4 mice) treated with negative control (Fc); “PBS” represents the group (n = 4 mice) with EAE stimulation and PBS treatment; and “abN48-2-IgG1” represents the group (n = 4 mice) with EAE stimulation and abN48-2-IgG1 treatment (7.5 mg kg−1). “SB225002” represents the group (n = 4 mice) with EAE stimulation and daily treatment with CXCR2-selective inhibitor SB225002 (0.5 mg kg-1). For panel b to d, data are presented as mean (center) ± s.d. (error bars). For panel e, data are presented as dots overlapped with mean (column) ± s.d. (error bars). Two-tailed t-test was employed for the significance of differences. p < 0.0001 (p < 0.0001, ****) for t-test of “PBS” vs. “Naive” and “abN48-2-IgG1” vs. “PBS”, p = 0.0001 (p < 0.001, ***) for t-test of “abN48-2-IgG1” vs. “SB225002”. t-values and degree of freedom were referred to the “Methods” section.
