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Fig. 1 | Journal of Neuroinflammation

Fig. 1

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

Fig. 1

Complement activation in MS grey matter lesions. Complement expression was investigated in cortical (a) and subcortical (b, c) grey matter characterised by anti-myelin oligodendrocyte glycoprotein (MOG) and anti-HLA-D immunochemistry, to reveal demyelinated lesions (lesion edge marked by arrows in a–c) and activated microglia, in the absence of amoeboid macrophages (d). Complement C1qA mRNA (red-brown reaction product) was expressed in MS cortical grey matter neurons (NeuN+, blue; e), whilst complement activation fragment C3b-iC3b (hereafter referred to as C3b+) was localised to the membrane and cytoplasm of neurons and glia (cell-associated immunolabelling noted by arrows, f). Quantitative analysis of the density of C3b+ cells in cortical, deep grey matter and hippocampus from MS, non-MS inflammatory control and non-neurological controls (g). C3b+ cell density was increased in cortical and deep grey matter lesions in comparison to area-matched non-neurological controls (g). The proportion of C3b+ cells with a neuronal morphology was increased in MS cortex in comparison to non-neurological control (h). Anti-C3b immunolabelled myelin closely associated with a HLA+ macrophage (i), oligodendrocytes (j) and microglia (k). Abbreviations: Ctrl non-neurological control cohort, IC non-MS inflammatory controls, GMN grey matter normal, GML grey matter lesion. Each data point represents the mean value per area of interest (lesion, normal-appearing or control) for the respective grey matter field, per case. Group means and 95 % confidence interval are plotted and compared by Kruskal-Wallis and Dunn’s multiple comparison post-test. Scale bars: ac, 2 mm; df, 50 μm; ik, 5 μm

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