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Fig. 1 | Journal of Neuroinflammation

Fig. 1

From: Blockade of sustained tumor necrosis factor in a transgenic model of progressive autoimmune encephalomyelitis limits oligodendrocyte apoptosis and promotes oligodendrocyte maturation

Fig. 1

TNF blockade limits demyelinating lesion size coincident with ameliorated astrocyte and myeloid cell reactivity during progressive EAE in GFAPγR1Δ mice. a Representative confocal Z-stack images depicting fluoromyelin staining of longitudinal spinal cord sections from WT and GFAPγR1Δ mice treated either with isotype control (GFAPγR1Δ) or anti-TNF mAb (GFAPγR1Δ + αTNF) during acute (d19 p.i.) and chronic EAE (d30 p.i.). Demyelinated areas identified by loss of fluoromyelin staining are delineated by dotted white line. Scale bar, 50 μm. b Quantification of lesion size (mm2) per field of view in WT (black), GFAPγR1Δ (red), and GFAPγR1Δ + αTNF (blue) mice during acute (d19 p.i.) and chronic EAE (d30 p.i.). Each symbol represents one lesion, with n compiled from three to four fields per mouse with five to six mice per group from two to three independent experiments. c Astrocyte (GFAP) and d macrophage/microglia (Iba1) positive area per square micrometer demyelinating lesion area. n = 3–4 fields per mouse with 2–3 mice per group. Total numbers of e macrophages (CD45hi CD11b+) and f microglia (CD45int CD11b+) in the CNS of all three mouse groups at d30 p.i. assessed by flow cytometry. Data represents mean ± SEM from pooled samples of five mice per group per experiment, three to four independent experiments per group. P values were determined by Student’s t test. GFAPγR1Δ in all panels represents GFAPγR1Δ mice treated with isotype control mAb

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