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. Author manuscript; available in PMC: 2011 Apr 11.
Published in final edited form as: Immunity. 2010 Mar 18;32(3):414–425. doi: 10.1016/j.immuni.2010.03.004

Figure 5. Endothelial-derived Act1 is dispensable for EAE development.

Figure 5

(A) Immunofluorescent staining of CD4+ T cells relative to the vasculature in the spinal cord. Spinal cords of wild-type and Act1−/− mice transferred with MOG-specific Thy1.1+ Th17 cells (n=3, 12 days after T cell transfer) were stained with CD4 (green) and pan-laminin (red) antibodies. The presented data is a representative of three independent experiments. (B) Real-time PCR for the Act1 expression in PECAM-1+ heart endothelial cells from endothelial-specific Act1-deficient (TIE2eCreAct1fl/−) and control mice (TIE2eCreAct1fl/+). (C) Mean clinical score of EAE in TIE2eCreAct1fl/− and TIE2eCreAct1fl/+ induced by active immunization with MOG35-55 (n=5/group). (D) Mean clinical score of EAE in TIE2eCreAct1fl/− and TIE2eCreAct1fl/+ mice induced by MOG-specific wild-type Th17 cells. (E) Flow cytometry analysis of immune cell infiltration in the brains of MOG35-55 immunized TIE2eCreAct1fl/− and TIE2eCreAct1fl/+ mice (n=5, 14 days after disease onset). Error bars, SEM; *, p<0.05.