Figure 1. Aggravation of EAE in mice cured from malaria correlates with increased cellular immune response towards myelin.

C57BL/6 mice (n = 6 mice/group) were intraperitoneally (i.p.) infected with 1×10⁶ P.berghei-infected Red Blood Cells and treated with chloroquine (CQ, 5 mg/Kg) for five consecutive days starting at the 10^th day after infection. Three days after the last dose of CQ, mice were immunized with 100 µg of MOG_35–55 peptide and Pertussis toxin was administrated (via i.p.) at 0 and 48h after peptide immunization for EAE induction. A) The clinical course of EAE was then monitored. Linear regression analyses are exposed in the side panels, thinner lines indicate 95% confidence interval. B) At the 10^th day after MOG-immunization, the spleens of mice were collected and dissociated. Total leukocytes (5×10⁵/well) were CFSE-stained (2,5 µM) and cultured in the presence of MOG_35–55 (10µg/mL) peptide for 96h. At the end of culture period, the cells were surface stained with anti-CD3/CD4/CD8 antibody cocktail and events were acquired in a flow cytometer. The proliferation was analyzed inside each T cell population. C) The culture supernatants were assayed for the secreted cytokines IL-10, IL-4, IL-6, IL-17, TNF-α and IFN-γ. Data was analyzed by One-Way Anova and post-tested with Bonferroni. In all analyses, *: p<0,05; ns: not significant. Representative data of three independent experiments.