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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Complement is activated in progressive multiple sclerosis cortical grey matter lesions

Fig. 2

Classical, alternative and terminal complement pathway activation in MS cortical lesions. Control (a) and MS cortex (bd) 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: ad, 2 mm; eg, 100 μm

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