Skip to main content
Fig. 5. | Journal of Neuroinflammation

Fig. 5.

From: Anti-MOG autoantibodies pathogenicity in children and macaques demyelinating diseases

Fig. 5.

Immunohistology of brain lesions of macaque EAE. ac Tissue sections from brain lesions were stained to detect IgG, IgM, and the myelin protein MBP (confocal microscopy) or the marker of activated microglia/macrophages IBA1 or the complement factor C1q (bright field microscopy). (scale bars 20 μm). a Immunofluorescence (IF) staining of MBP in green and IgM in red shows the non-overlapping presence of MBP and IgM; inset: a higher magnification shows a microglia/macrophage coated with IgM and containing MBP. b IF of MBP in green and IgG in red, shows colocalized MBP and IgG; inset: a higher magnification shows a microglia/macrophage with MBP-positive myelin particles colocalized with IgG. c Intralesional presence of C1q (brown precipitates) within neutrophils and microglia/macrophages; left inset: a higher magnification of an activated microglia/macrophage labeled with IBA1, right inset: a higher magnification of a macrophage with intracytoplasmic labeling of C1q. dh Prephagocytic lesions in macaque EAE detected as myelin vacuolization in a lesion proximal to an active demyelinating lesion in the white matter in the subcortical area of a macaque brain (bright field microscopy, scale bars 50 μm). d HE stains shows evenly distributed brain cells in the white matter and myelin vacuolization and the absence of leukocyte infiltrate. e Diffuse IgG deposits surrounding the white matter. Inset shows that the myelin in immediate proximity of this prephagocytic lesion is free of IgG labeling. f Diffuse C1q deposition on vacuolized myelin. g The same area shows the presence of widespread and perivascular IBA1+ activated microglia. h In these lesions, normal GFAP expression indicates absence of astrogliosis

Back to article page