Fig. 3: CXCR1 deficiency in DC ameliorates EAE progression.

WT or DC conditional knockout mice (DC (WT) or DC (Cxcr1^−/−)) were immunized with MOG_35–55 peptides in CFA adjuvant and pertussis toxin to induce EAE. A Mean clinical scores of EAE in DC (WT) and DC (Cxcr1^−/−) mice (left panel), and linear regression analysis (right panel) of the recipient mice depicted (n = 5). The data are expressed as the mean ± SEM. ^*p < 0.05, vs. DC (WT) group (Mann–Whitney U test). B Representative flow cytometry data showing intracellular production of IFN-γ and IL-17A in CD4⁺ T cells from the spinal cord and brain of DC (WT) and DC (Cxcr1^−/−) mice 28 days after EAE induction. Pooled data are presented in the right panel. C H&E staining and LFB staining (D) of spinal cord paraffin sections from the DC (WT) and DC (Cxcr1^−/−) mice 28 days after EAE induction. Scale bars, 200 μm. Pooled data are presented in the right panel. E IL-12p70, IL-6, and TGF-β1 levels in the serum of DC (WT) and DC (Cxcr1^−/−) mice 12 days after EAE induction were detected by ELISA. F Expression of Il12a, Il6, and Tgfb1 mRNA in the spinal cord and brain from the DC (WT) and DC (Cxcr1^−/−) mice 28 days after EAE induction. Data are mean ± SEM. ^*p < 0.05, ^**p < 0.01, ^***p < 0.001 vs. DC(WT) group (one-tailed Student’s t-test).