BMMØ deficient in both cathepsins B and S have reduced MHC-II surface expression and presentation of MOG antigens, and mice deficient in both cathepsins B and S are protected from EAE.

<p>(A-C) WT and cathepsin B and S (Cat B^-/-S^-/-) deficient BMMØ were (A) examined for their MHC-II surface expression (I-Ab, quantified by MFI), or their ability to activate MOG^35-55-specific CD4+ T cells following incubation with (B) MOG^35-55 peptide (0, 10, 25 μg/ml) or (C) MOG^1-125 (0, 10, 25 μg/ml). Activation of MOG^35-55-specific 2D2 CD4+ T cells was determined by surface expression of CD69 after 16 h incubation with the BMMØ (n = 4). (D) Clinical disease course and (E) number of days to clinical onset (score of at least 0.5) of WT and Cat B^-/-S^-/- deficient mice after active induction of EAE with 50μg MOG^35-55 in CFA (day 0) and 300 ng pertussis toxin (day 0 and 2), (N = 8). (F) The number of macrophages (MØ, CD11b+/CD45 high), microglia (MG, CD11b+/CD45 low), CD4+ T cells (CD4+/CD3+), and CD8+ T cells (CD8+/CD3+) isolated from the spinal cord (via a discontinuous percoll gradient) of mice 18 days following inoculation with MOG^35-55 (n = 3). Data presented as mean+/- SEM; significant differences (Clinical data, Mann-Whitney Test; unpaired students t-testp<0.05) from the WT internal control are denoted by asterisks (*).