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 [Go to this article.]

Figure 6
Cannabinoid treatment inhibits mRNA coding for both antiviral and Th1- and Th2-type inflammatory mediators in the CNS. R(+)WIN55,212 treatment at the time of infection (day 0–5) inhibited spinal cord mRNA coding for the innate antiviral mediators, IFN-α, and IFN-β (a). R(+)WIN55,212 treatment at the onset of disease inhibited spinal cord mRNA coding for the proinflammatory Th1 mediators, IL-1β, IL-6, TNF-α, and IFN-γ, but not the IL-12 p40 subunit (b). Treatment at disease onset also inhibited mRNA coding for the Th2 cytokine IL-4, but not IL-10 (c). The mRNA levels are presented as the percentage of intensity of the HPRT control for that sample.