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Fig. 5 | Journal of Neuroinflammation

Fig. 5

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

Fig. 5

Mice deficient in cathepsin Z have dramatically reduced circulating IL-1β during EAE and attenuated Th17 responses in vivo; consistently, APCs deficient in cathepsin Z are unable to efficiently generate IL-1β and IL-18 in vitro. a Proinflammatory cytokine levels in WT and Cat Z−/− EAE serum 15 days post induction (n = 3–6). b The percentage of Th1 (IFNγ+), Th17 (IL-17+), and FoxP3+ CD4+ T cells isolated from the inguinal lymph nodes of WT and Cat Z−/− mice 6 days after injection with CFA (n = 3). c, d Concentration of IL-1β within the supernatant of WT and Cat Z−/− (c) BMMØ, and (d) BMDC after priming with LPS and subsequent exposure to NLRP3-inflammasome activators (c) monosodium urate (MSU) or (d) ATP as quantified by ELISA (n = 5). e, f Concentration of IL-18 within the supernatant of WT and Cat Z−/− (e) BMMØ, and (f) BMDC after priming with LPS and subsequent exposure to the NLRP3-inflammasome activators (e) MSU or (f) ATP as quantified by ELISA (n = 5). g, h IL-1β mRNA levels of WT and Cat Z−/− (g) BMMØ and (h) BMDCs stimulated with LPS as determined by qPCR (n = 3–5). Data presented as mean +/− SEM; significant differences (unpaired Student’s t test, p < 0.05) from the WT control are denoted by asterisks

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