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. 2016 Mar 9;3(2):e212. doi: 10.1212/NXI.0000000000000212

Figure 1. Influence of B-cell very late antigen-4 (VLA-4) deficiency on experimental autoimmune encephalomyelitis (EAE) induced by recombinant extracellular domain of human myelin oligodendrocyte glycoprotein protein (rhMOG) or myelin oligodendrocyte glycoprotein (MOG) p35-55.

Figure 1

(A) CD19cre/α4f/f (n = 24 mice) and control mice (n = 23 mice) were immunized with 100 μg rhMOG. (B) CD19cre/α4f/f (n = 16 mice) and control mice (n = 14 mice) were immunized with 100 μg MOG p35-55. Cumulative data from 2 independent experiments are shown in (A) and (B). Results represent mean disease score ± standard error of the mean. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; Mann-Whitney U test. Serum immunoglobulin G (IgG) antibodies against MOG p35-55 (C) and rhMOG (D) were detected by ELISA. Values represent optical density (OD) at 450 nm. CD19cre/α4f/f or control mice (n = 3 mice/group) were immunized with 100 μg MOG p35-55 (C) or 100 μg rhMOG (D). Serum, collected at the end of the experiment, was diluted 1:300 (C, left panel) or 1:9,000 (C, right panel, D) before analysis. ns = not significant; unpaired t test with Welch correction.