Figure 3. Rras-deficiency in the periphery, but not in the CNS, results in attenuated EAE severity.

A,B, chimera mice in which either the CNS and peripheral radioresistant cells (WT→Rras^−/−) or the peripheral immune cells (Rras^−/−→WT) were deficient in R-Ras were generated by transplanting lethally irradiated Rras^−/− (A) or WT (B) recipient mice with WT (A) or Rras^−/− (B) BM cells. Control chimeras were generated by transplanting WT BM into WT mice (WT→WT) (A,B). Ten weeks after BM reconstitution, EAE was induced by immunization with MOG_35-55 peptide and EAE disease was scored daily starting on day 7. Representative data of two independent experiments with five mice in each group (A) or data from one experiment with six mice in the WT→WT and four mice in the Rras^−/−→WT group are shown (B). C, EAE was induced in WT or Rras^−/− mice with MOG_35-55 peptide and seven days later purified CD4⁺ cells from the draining BLN were stimulated in vitro with varying concentrations of MOG_35-55 peptide and their proliferation was determined by CFSE dye dilution by flow cytometry. Dead cells were excluded using DAPI. Percentages of proliferating CD4⁺CD11b⁻DAPI⁻ cells at different concentrations of MOG_35-55 peptide are shown. Pooled data from three independent experiments with six mice in each group are shown. ***p<0.001.