Immunoregulation of a viral model of multiple sclerosis using the synthetic cannabinoid R(+)WIN55,212
J. Clin. Invest. J. Ludovic Croxford, et al. 111:1231 doi:10.1172/JCI17652 [
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Figure 3Effects of cannabinoid receptor agonism on T cell proliferation depends upon the cellular activation state. Early R(+)WIN55,212 treatment (filled circles) (postinfection day 0–5) significantly inhibited the proliferation of T lymphocytes compared with S(–)WIN55,212 (open circles) and untreated TMEV-infected mice (filled triangles) upon rechallenge with the TMEV VP2
70-86 peptide (postinfection day 8) (
a), but not PLP
139-151 (
d). When measured at postinfection day 40, R(+)WIN55,212 treatment did not inhibit T lymphocyte proliferation to either VP2
70-86 or PLP
139-151 peptides during established disease (postinfection day 26–31 or 50–55) (
b,
c,
e, and
f). *
P < 0.05, compared with either S(–)WIN55,212 or untreated mice.
