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. 2017 Oct 18;8:1364. doi: 10.3389/fimmu.2017.01364

Figure 4.

Figure 4

Complement deposition in LGI1 antibody-positive FEPSO animals. Staining for early constituent, C1q of the complement cascade shows the absence of C1q on neurons of (A) the hippocampus of a normal control and (B) the hippocampus of an epileptic control animal. (C) The hippocampus of a FEPSO cat shows C1q reactivity on the surface of hippocampal neurons with occasional granular staining inside the cells (inset). (D–K) The brain areas affected by BBB leakage are also affected by complement activation as shown by immunohistochemistry for C9neo. (D) In the hippocampus, complement-positive cells are visible, which show a [(G), enlargement] granular staining pattern inside the cells. (E) The amygdala shows very similar staining with C9neo positive cells, which [(H), enlargement] show the same granular staining inside the cells. Neither (F) the basal ganglia, (I) cortex, (J) cerebellum nor (K) white matter showed any complement positive cells or structures. (L) Quantification of C9neo positive cells revealed significantly higher numbers in the hippocampus as well as in the amygdala. Data shown as median with interquartile range, LGI1 antibody-positive animals are indicated in red, and untested animals in black (*p < 0.05, Kruskal–Wallis test with Dunn’s post hoc correction, hippocampus n = 15, amygdala n = 9, basal ganglia n = 12, cortex n = 15, cerebellum n = 13). Scale bars correspond to (A,B,D,E) 100 µm, (C) 50 µm, (G,H) 20 µm, (F,I,K) 25 µm, and (J) 200 µm.