Fig 2: CB1 and CB2 expression, represented as median fluorescence intensity (left panel) in PBMC from 12 healthy controls and 12 MS patients under the specified stimulation conditions. Data are shown for lymphocyte/monocyte-gated cells. The right panel is a representative histogram of CB 1 and CB 2 expression in an MS patient's PBMCs in different stimulation conditions. Colour legend, Black: Isotype Control; Red: Unstimulated; orange: +IL-1ß; blue: +IL-6; pink: +TNF-a. Results show a statistically significant increase in CB 2 expression between controls and MS patients after stimulation with IL-1ß, IL-6, and TNF-a.

Fig 3: (a–b) CB1 and CB2 protein expression determined by flow cytometry. Changes were measured as increase in mean fluorescence intensity (MFI) of gated lymphocytes/monocytes (a) CB1 and CB2 in whole blood (left panel). (b) CB1 and CB2 in PBMC (right panel). See, text for significance levels. Results shown are representative of five independent experiments. Control = rabbit IgG.

Fig 4: Comparison of the relative expression level of Cnr1 and Cnr2 in equine brain (Eq. Brain); skin (Eq. Skin); keratinocytes (Eq. Keratinocytes) and fibroblasts (Eq. Fibroblasts). The transcript level in each biological sample is displayed as the mean value of 2-?CT ± SEM

Fig 5: (a) a1. Densitometry graph of the Western blots (n = 3) for CB1 at 60 kDa. a2. Western blots showing immunoreactivity to CB1 antibody. Bands were detected at 32 (not shown) and 60 kDa corresponding to CB1. Lower blot (a2) is the corresponding ß-actin. (b) b1. Densitometry graph of the Western blots (n = 3) for CB2. b2 shows 60 kDa band for CB2 and below; lower blot (b) is its corresponding ß-actin. TNF-a increased CB2 levels (OD avg = 0.34 ± 0.07; 17% increase), which was reduced in the presence of receptor antagonists (OD avg = 0.27 ± 0.07). TNF-a increased CB1 (OD avg = 0.65 ± 0.13; 55% increase; P < 0.025). No changes in corresponding ß-actin were observed.