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Fig. 3 | Journal of Neuroinflammation

Fig. 3

From: CXCR3 signaling in glial cells ameliorates experimental autoimmune encephalomyelitis by restraining the generation of a pro-Th17 cytokine milieu and reducing CNS-infiltrating Th17 cells

Fig. 3

A CXCR3-deficient CNS milieu is responsible for the higher susceptibility of CXCR3−/− mice to EAE. Splenocytes isolated from MOG-immunized WT or CXCR3−/− mice on day 10 post-immunization were cultured under Th17-polarizing conditions in the presence of MOG, IL-6, IL-23, and TGF-β for 72 h. Cultured CD4+ T cells were purified by MACS-positive selection, and 3 × 105 CD4+IL-17+ cells were transferred into irradiated (4 Gy) WT or CXCR3−/− mice followed by immunization with a suboptimal dose of MOG/CFA (10 μg/50 μg) and injection of PTX (200 ng/ml; day 0 and day 2). Four adoptive-transfer EAE experiments were performed: (1) WT (Th17) → WT, (2) WT (Th17) → CXCR3−/−, (3) CXCR3−/− (Th17) → WT, and (4) CXCR3−/− (Th17) → CXCR3−/−. Survival rates of recipient WT and CXCR3−/− mice at various times post-immunization are shown. a Comparison of transfer of polarized Th17 cells with different origins into WT recipient mice (WT → WT vs. CXCR3-/- → WT, left panel) or CXCR3−/− recipient mice (WT → CXCR3−/− vs. CXCR3-/- → CXCR3−/−, right panel). b Comparison of transfer of polarized Th17 cells with the same origins into WT or CXCR3−/− recipient mice (WT → WT vs. WT → CXCR3−/−, left panel; CXCR3−/− → WT vs. CXCR3−/− → CXCR3−/−, right panel). Data shown are from two independent experiments (12 mice for each adoptive-transfer EAE group). *P < 0.05; **P < 0.01; ***P < 0.001

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