Fig. 1
From: Complement is activated in progressive multiple sclerosis cortical grey matter lesions

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: a–c, 2 mm; d–f, 50 μm; i–k, 5 μm