ELR⁺ CXC chemokines partially compensate for loss of G-CSF signaling in Csf3r^−/− adoptive transfer recipients. (A–G) WT (closed triangles, black bars) and Csf3r^−/− (open triangles, white bars) mice were injected with MOG-specific Th17 cells. (A) Mean clinical scores, representative of seven independent experiments (n ≥ 7 mice per group). (B) Absolute number of neutrophils, monocytes, and microglia recovered from the spinal cord on day 7 after transfer, assessed by flow cytometry (n ≥ 7 per group, pooled from two experiments). (C) Number of neutrophils per milliliter of blood or per spleen at baseline and on day 7 d after transfer, assessed by flow cytometry (n ≥ 7 per group, pooled from two experiments). (D) Fold change in the number of circulating and splenic neutrophils over baseline on day 7 after transfer. (E) Proportion of donor cells expressing IL-17 and IFN-γ immediately before adoptive transfer, and after isolation from the spinal cords of WT or Csf3r^−/− hosts on day 7 after transfer (n = 5 per group). (F) Levels of CXCL1 in sera from naive mice and adoptive transfer recipients, measured by ELISA (n ≥ 9, pooled from three experiments). (G) CXCL1 levels in spinal cord homogenates were measured by ELISA and normalized to total protein (n ≥ 4). (H) Csf3r^−/− recipients of WT Th17 cells were treated with control serum (n = 7) or anti-CXCR2 (n = 6) every other day from days 0– 8 (arrows). Data are representative of two independent experiments. All graphs indicate means; error bars denote SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001.