Fig. 1: CXCR1 deficiency suppresses EAE development.

A CXCR1 mRNA expression in peripheral blood leukocytes in healthy controls (n = 21) and MS patients (n = 35) (left panel). Scatterplots showing the correlation between mRNA level of CXCR1 and EDSS in MS patients (right panel). WT and Cxcr1^−/− mice were immunized with MOG_35–55 peptides in CFA adjuvant and pertussis toxin to induce EAE. B Clinical scores of EAE in immunized WT and Cxcr1^−/− mice (left panel), and linear regression analysis (right panel) of the recipient mice depicted (n = 6). The data are expressed as the mean ± SEM. ^*p < 0.05, vs. WT group (Mann–Whitney U test). C H&E staining and LFB staining of spinal cord paraffin sections from the WT and Cxcr1^−/− mice 28 days after EAE induction. Scale bars, 200 μm. D Pooled data are presented from (C). E Representative flow cytometry data showing intracellular production of IFN-γ and IL-17A in CD4⁺ T cells from the spinal cord and brain of WT and Cxcr1^−/− mice on 28 days after EAE induction. Pooled data are presented in the right panel. F ELISA analysis of cytokines (IL-12p70, IL-6, and TGF-β1) in the serum from WT and Cxcr1^−/− mice 12 days after EAE induction. G mRNA levels of Il12a, Il6, and Tgfb1 in the brain from WT and Cxcr1^−/− mice on days 0 and 21 after EAE induction. H ELISA analysis of IL-6, IL-12p70, and TGF-β1 in supernatant of DCs sorted from WT and Cxcr1^−/− mice 12 days after EAE induction and restimulated with MOG_35–55 for 48 h. Data are mean ± SEM. ^*p < 0.05, ^**p < 0.01, ^***p < 0.001 vs. WT group (one-tailed Student’s t-test). Data are representative of three independent experiments with similar results.