Vav1^R63W mice are less susceptible to EAE.

<p>(A) EAE was induced in mice by immunization with MOG_35-55 peptide, using either 50 μg (upper panels, n = 10) or 100 μg (lower panels, n = 32). Disease severity was monitored daily. Histograms show mean cumulative scores, onset day and maximal score for the indicated genotypes. (B, C) Histograms show the mean absolute numbers of CD4 T cells and CD4⁺Foxp3⁺ Treg cells in the brain (B) and spinal cord (C) at the peak of the disease (day 15, n = 7 to 9 mice per group). Cells were re-stimulated overnight with MOG_35-55 and cytokine expression was analyzed by intracellular staining in CD4 T cells from the brain (B) and spinal cord (C). (D, E) Tetramer staining showing CD4⁺CD44⁺ T cells specific for the MOG_35-55 peptide in the brain (D, middle panels), spinal cord (D, lower panels) and LN (E) of WT (n = 6) and Vav1^R63W (n = 6) mice at day 15 after immunization. The tetramer staining showing CD4⁺CD44⁺ T cells specific for the CLIP peptide is used as control. Graphs show the mean percentages and absolute numbers of CD4⁺CD44^highTetramer⁺ cells for the indicated genotypes. Results are representative of two independent experiments. ■: Vav1^R63W mice; □: WT mice; *p≤0.05; **p≤0.01; ***p≤0.001.