Fig. 2

Classical, alternative and terminal complement pathway activation in MS cortical lesions. Control (a) and MS cortex (b–d) immunostained for MOG and HLA-D to reveal lesions affecting the deeper cortical laminae (b, c, arrows indicate lesion edge of a type I and type IV lesion, respectively) and a subpial lesion (d). Within an active cortical grey matter lesion (e–e′′ arrows indicate lesion edge in e and e′ and early myelin degradation products in e′′), C1q+ and C3b+ immunostaining was noted (arrows indicate labelled cells. Note the total absence of C3b immunolabelling of a neuron directly adjacent to a C3b+ cell (e′′). Immunolabelling of cells morphologically resembling neurons and glia in the deep cortical laminae of control and MS lesions indicated activation of the classical (C1q+, f, f′), alternative (fragment Bb+, g, g′) and terminal (C9neo+, h, h′) complement pathways (arrows in insets in f′–h′ highlight immunopositive neurons or glia). The numerical density of C1q+ (i), fragment Bb+ (j) and C9neo+ (k) cells was increased in grey matter and white matter lesions. Each data point represents the mean value per area of interest per case and group means and 95 % confidence intervals plotted. Groups were compared by Kruskal-Wallis and Dunn’s multiple comparison post-test. Scale bars: a–d, 2 mm; e–g, 100 μm