Figure 6
Figure 6. Modulation of p38 MAPK activity specifically in T cells influences EAE susceptibility and severity. (A) Clinical course of EAE in WT B10.BR and dn-p38-Tg mice immunized with 1× MOG97-114-CFA + PTX. (B) Clinical course of EAE in WT and MKK6-Tg mice immunized with 1× MOG97-114-CFA + PTX. (A-B) Significance of the differences in the clinical course of disease was determined by regression analysis and the best-fit curves are shown. (C-D) EAE was induced in WT (n = 29) and MKK6-Tg (n = 8) mice by immunization with 1× PLP190-209-CFA + PTX. The incidence (C) and the cumulative disease score (CDS; D) are shown. The significance of the differences was determined using the independent samples t test within SPSS (Levene test for equality of variances and t test for equality of means; ***≤ 0.001).

Modulation of p38 MAPK activity specifically inT cellsinfluences EAE susceptibility and severity. (A) Clinical course of EAE in WT B10.BR and dn-p38-Tg mice immunized with 1× MOG97-114-CFA + PTX. (B) Clinical course of EAE in WT and MKK6-Tg mice immunized with 1× MOG97-114-CFA + PTX. (A-B) Significance of the differences in the clinical course of disease was determined by regression analysis and the best-fit curves are shown. (C-D) EAE was induced in WT (n = 29) and MKK6-Tg (n = 8) mice by immunization with 1× PLP190-209-CFA + PTX. The incidence (C) and the cumulative disease score (CDS; D) are shown. The significance of the differences was determined using the independent samples t test within SPSS (Levene test for equality of variances and t test for equality of means; ***≤ 0.001).

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