Fig. 6
From: Claudin-12 is not required for blood–brain barrier tight junction function
Absence of claudin-12 does not affect BBB integrity nor aggravate the development of EAE. a Graph of the clinical disease course of one representative MOGaa35-55 induced aEAE in WT (black line; n = 11) and claudin-12lacZ/lacZ C57BL/6J mice (blue line; n = 11) is shown. Average disease scores ± SEM as assessed twice daily are shown. b Disease severity determined by the area under the curve (AUC) and analyzed until day 55. Bar graphs represent the mean ± SD of two independent experiments including 21 WT and 21 claudin-12lacZ/lacZ C57BL/6J mice. c Immunofluorescence staining for fibronectin (green) and mouse IgG (red) on frozen brain sections from WT and claudin-12lacZ/lacZ C57BL/6J is shown. Upper row—healthy mice, lower row mice suffering from EAE. Two independent stainings were performed. Scale bar = 50 μm. d Immunohistochemical staining of frozen brain sections from WT and claudin-12lacZ/+ C57BL/6J mice after induction of aEAE. β-galactosidase (blue) staining can be seen in examples of the cortex, cerebellum and choroid plexus. Animals with score 0 were induced with aEAE but did not develop any clinical symptom, whereas animals with score 2 presented hindleg paraplegia. Three independent stainings were done. Scale bar = 50 μm