Glia-dependent TGF-β signaling, acting independently of the TH17 pathway, is critical for initiation of murine autoimmune encephalomyelitis
J. Clin. Invest. Jian Luo, et al. 117:3306 doi:10.1172/JCI31763 [Go to this article.]

Figure 3
Early activation of TGF-β signaling in brains of SBE-luc (A) or SBE-lucRT (B–H) mice after immunization. (A) Time course showing bioluminescence signals indicative of TGF-β signaling in a representative SBE-luc mouse. (B–H) Activation of TGF-β signaling indicated by reporter gene expression in neurons and infiltrating lymphocytes. SBE-lucRT mice were immunized with MOG_35–55 and adjuvants (C–E) or injected with PBS as control (B). (B–E) Sagittal brain sections were stained for RFP, and images were taken from the cerebellum granule cell layer. (F–H) Confocal microscope images of double immunolabeling with antibodies against RFP (green) and cell type–specific markers (red): CD68 (microglia, F), GFAP (astrocyte, G), and CD4 (T cell subset, H). RFP-expressing cells appear yellow after superimposition. Sections were from a mouse sacrificed at 14 dpi (D–E). Scale bars: 50 μm (A–E); 20 μm (F–H). Insets in H show RFP-expressing CD4⁺ T cells in cerebellum parenchyma. Scale bar: 20 μm.