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. Author manuscript; available in PMC: 2014 Jun 15.
Published in final edited form as: J Immunol. 2013 May 17;190(12):6004–6014. doi: 10.4049/jimmunol.1203552

Figure 1. Oral Ig-MOG diminishes Th1 and Th17 responses and reverses EAE.

Figure 1

Groups of 6- to 8-wk-old C57BL/6 mice were induced for EAE with MOG peptide (MOG EAE) or CNS homogenate (CNS EAE). Seven days later, the mice were treated orally with 300 μg sol (A) or agg (B) Ig-MOG or Ig-W and 1 mg soy trypsin inhibitor (STI) for four times at 2-day intervals. Mice recipient of STI alone (STI) were included for control purposes. Mice were monitored daily for clinical signs of disease. Data is representative of three individual experiments with 5 mice per group. (C) Mice were induced for MOG EAE and treated orally with agg Ig-MOG +STI or STI alone (STI) as in B. Mice were sacrificed 15 days after the last treatment (day 21 peak of disease) and their mesenteric lymph node (MLN), lamina propria (LP), and peripheral lymph node (PLN) including axial and popliteal were harvested and the cells were re-stimulated in vitro with free MOG peptide for 48 hours. IFNγ (top row) and IL-17 (bottom row) cytokine production was analyzed by ELISA. PLP1 peptide was included for control purposes. Data is representative of three individual experiments. Each bar represents the mean ± SD of triplicate wells. * p<0.005