Fig. 1
Design and treatment effects of the DRα1-mMOG-35-55 construct in acute EAE: a Design, sequence and ribbon model of the DRα1-mMOG-35-55 construct. b Treatment of acute EAE in DR*1501-Tg mice with 5 daily doses of vehicle or 100 μg DRα1-mMOG-35-55 starting at a score of ≥ 2 reduced daily (**p < 0.01) and cumulative (***p < 0.001) disease scores and c spinal cord histological damage (red) and demyelination as visualized after toluidine blue staining (scale bar 100 mm). High-power view of small areas of lumbar spinal cord (black rectangles) show axons that are undergoing demyelination (red arrow) and cellular infiltration (red arrowhead). Scale bar is 10 mm. d DRα1-mMOG-35-55 treatment of C57BL/6 male mice with EAE reduced the absolute numbers of lymphocytes, CD11b+CD45high myeloid cells, and CD3+ T cells in the spinal cord and brain, expression of CD74 on CD11b+CD45high spinal cord cells and intracellular expression of CD4+IL-17+ T cells in the brain (after stimulation with PMA and ionomycin) and increased the frequency of CD206+CD11b+CD45hi cells in spinal cords. e DRα1-mMOG-35-55 treatment reduced the relative expression of pro-inflammatory genes (CD74, NLRP3, and IL-1b) and increased the expression of genes involved in neurosurvival and regeneration (HUWE1, MBP, and HDAC5) in spinal cord samples from C57BL/6 male mice. *p < 0.05, **p < 0.01, ***p < 0.001. Panels (a) (partial), (b, d, and e) reprinted [adapted] from “HLA-DRα1-mMOG-35-55 treatment of Experimental autoimmune encephalomyelitis reduces CNS inflammation, enhances M2 macrophage frequency, and promotes neuroprotection,” by Benedek et al., 2015, Journal of Neuroinflammation, 12:123, Biomedical Central, copyright Benedek et al. 2015 [28]. Reprinted with permission. Published with original ribbon graphic of the DRα1-MOG-35-55 construct. Panel (c) reprinted from “HLA-DRα1 constructs block CD74 expression and MIF effects in experimental autoimmune encephalomyelitis,” by Meza-Romero et al., 2014 [22]. Journal of Immunology, 192(9):4164-73, copyright of The American Association of Immunologists. Reprinted with permission