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. 2013 Oct 28;191(11):5441–5450. doi: 10.4049/jimmunol.1301188

FIGURE 6.

FIGURE 6.

HuR is required for initiation of EAE. Splenocytes and lymph node cells from immunized control and HuR KO mice were cultured in the presence of MOG35–55 (20 μg/ml) and murine IL-23 (20 ng/ml) for 3 d. CD4+ T cells were isolated, and 6 to 7 × 106 cells were injected i.v. into sublethally irradiated WT mice following two dosed pertussis toxin injections. (A) Disease onset in mice receiving adoptively transferred WT or HuR KO CD4+ T cells and observed until day 55 shows delay in disease initiation. Data in (A) and (B) were summarized for at least six mice per group and are representative of two independent experiments. (B) Development of clinical disease in early time points in recipients after adoptive transfer of WT control or HuR KO CD4+ Th17 polarized T cells. These data represent an independent experiment from (A). (C) Disease onset in mice. Data in (B) were summarized for at least six mice per group and representative of two independent experiments. Error bars in (A) and (B) represent ± SEM. (DG) Proinflammatory cells in spinal cord of recipients that received WT and HuR KO Th17 cells at day 21 after transfer were isolated and analyzed by flow cytometry. These data are representative of four pairs of mice from two independent experiments. *p < 0.05, **p < 0.01.