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. 2017 Feb 1;8:27. doi: 10.3389/fimmu.2017.00027

Figure 2.

Figure 2

Cylindromatosis (CYLD) augments brain pathology in experimental cerebral malaria. Histopathology of WT and Cyld−/− mice at day 7 postinfection (p.i.). (A) hematoxylin and eosin staining showing numerous hemorrhagic lesions scattered throughout the brain of WT mice at day 7 p.i. Pronounced activation of astrocytes (B) and microglia (C) in the brain of a WT mouse as shown by glial fibrillary acidic protein and ionized calcium–binding adaptor molecule 1 staining, respectively. (D) Strong immunostaining of MHC class I molecules on microglial cells in a brain of WT mouse. (E) Accumulation of CD8+ T cells in the brain of a WT mouse at day 7 p.i. (F) CD31 staining shows a prominent staining pattern on endothelial cells in the brain of a WT mouse. (G) Apoptosis of endothelial cells is visualized in the brain of a WT mouse by active caspase-3 staining in a vessel wall. (H) Double immunofluorescence shows co-localization of CD31+ endothelial cells (green) with active caspase 3 (red) in the brain of a WT mouse at day 7 p.i., while this is not found in a Cyld−/− mouse. Representative staining results of three independent experiments are displayed.