Figure 3

Cellular organization of preactive lesions. Preactive lesions were not associated with the cerebrovasculature (A: HLA-DR in green, glucose transporter protein-1 in red, arrows indicate vessels). No alterations were observed in the expression of the tight junction molecule claudin-5 (B: HLA-DR in red, claudin-5 in green, arrow indicates vessel), and fibrinogen immunoreactivity (C: HLA-DR in red, fibrinogen-FITC in green) was restricted to the lumen of the cerebrovasculature in areas with preactive lesions (C, arrow). Analysis on the expression of glial fibrillary acidic protein (D: HLA-DR in green, glial fibrillary protein in red) and neurofilament (E: HLA-DR in green, neurofilament in red), common markers for astrocytes and axons, respectively, demonstrated no signs of astrogliosis or axonal changes in or surrounding preactive lesions. Intra-axonal amyloid precursor protein accumulation, indicative of acute axonal injury, was absent in preactive lesions (F: APP in blue, HLA-DR in brown), but present in the rim of a chronic active MS lesions (G: APP in blue, HLA-DR in brown). T cell infiltrates were not associated with preactive lesions (H: CD3 in blue, HLA-DR in brown), but restricted to highly inflammatory areas (I: CD3 in blue, HLA-DR in brown). Original magnifications: A, C-F and H: 40×; B, G and I: 20×.