Fig. 1From: Blockade of sustained tumor necrosis factor in a transgenic model of progressive autoimmune encephalomyelitis limits oligodendrocyte apoptosis and promotes oligodendrocyte maturationTNF 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 mAbBack to article page