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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: A role for cathepsin Z in neuroinflammation provides mechanistic support for an epigenetic risk factor in multiple sclerosis

Fig. 2

Cathepsin Z expression is increased in the CNS during EAE, and mice deficient in cathepsin Z exhibit attenuated signs of neuroinflammation and demyelination during EAE. a Cathepsin Z mRNA levels in the spinal cord tissue of WT mice 15 days after induction of EAE or mock (n = 6). b Clinical disease course of WT and Cat Z−/− mice after active induction of EAE (n = 20–21). c Representative micrographs of transverse sections of lumbar spinal cord from WT and Cat Z−/− mice at 15 days after induction of EAE. Sections are stained with hematoxylin and eosin (HE) for inflammation, or Luxol fast blue (LFB) for demyelination. Grey and black scale bars indicate 500 and 100 μm respectively. d The total number of infiltrating macrophages (MO), B cells, CD8+ T cells (CD8+), CD4+ T cells (CD4+), and Th17 cells (IL-17+/CD4+) isolated from lumbar spinal cord tissue 15 days post EAE induction as analyzed by flow cytometry (n = 8–12). Data presented as mean +/− SEM; significant differences (unpaired Student’s t test; clinical data, Mann–Whitney U test; p < 0.05) from the WT control are denoted by asterisks

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