Fig. 3

IFNγ signaling directly regulates CXCR2 expression by neutrophils. a IFNγR-sufficient and IFNγRKO neutrophils (left panels) and monocytes/macrophages (right panels) were FACS sorted from the brainstems (upper panels), spinal cords (middle panels), and bone marrow (lower panels) of mixed bone marrow chimeric mice. CXCL2 transcript levels were measured by qPCR and normalized to GAPDH (n = 13 chimeric mice from two experiments). b CD45⁺CD11b⁺Ly6G⁺ neutrophils were FACS sorted from the spinal cord, brainstem, and bone marrow of WT mice at the onset of cEAE, and IFNγRKO mice at the onset of aEAE. Bone marrow cells from naïve mice were used as controls. CXCR2 mRNA levels were quantified by qPCR and normalized to GAPDH (n = 10 WT mice and 15 IFNγRKO mice with EAE, pooled from two experiments; n = 4 WT naive mice and 5 IFNγRKO naïve mice). c IFNγR-sufficient and IFNγRKO neutrophils (defined as CD45⁺CD11b⁺Ly6G⁺) were FACS sorted from the bone marrow, spinal cord, and brainstem of mixed bone marrow chimeric mice at the onset of EAE. CXCR2 transcript levels were normalized to GAPDH (n = 13 mice from two experiments)