Fig. 2

Impact of endothelial α5 integrin deletion on EAE development. a. Confirmation of the absence of α5 integrin expression in spinal cord endothelial cells in α5-EC-KO mice. Frozen sections of spinal cord taken from disease-free or pre-symptomatic EAE mice were processed for dual-IF for CD31 (AlexaFluor-488) and α5 integrin (Cy-3). Scale bar = 100 μm. Note that in contrast to WT spinal cord where strong upregulation of endothelial α5 integrin was observed, vessels in α5-EC-KO mice showed total lack of α5 integrin. b. The impact of endothelial α5 integrin deletion on clinical severity in EAE. The progression of EAE in α5-EC-KO and WT littermate control mice was evaluated by measuring clinical score on daily intervals. All points represent the mean ± SEM (n = 3 experiments, with 6–10 mice of each strain used per experiment). Note that compared to WT littermates, α5-EC-KO mice showed markedly earlier onset and faster progression of EAE. * p < 0.05 vs. WT.