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. Author manuscript; available in PMC: 2020 May 22.
Published in final edited form as: Toxicol Appl Pharmacol. 2019 Feb 23;369:82–89. doi: 10.1016/j.taap.2019.02.013

Fig. 3.

Fig. 3.

Treatment with THC, JWH-015, and JWH-133 inhibited the CpG-induced phosphorylation of the p65 subunit of NFκB and IKKγ (NEMO) in pDC. Isolated human PBMCs were treated with either Vehicle (VH; 0.03% Ethanol), CBD (10 μM), THC (0.1, 1, or 10 μM), JWH-015 (10−2, 10−1, 100 μM) or JWH-133 at (10−3, 10−2, 10−1 μM) for 30 min, stimulated with CpG-ODN at 15 μg/ml for 5 h and intracellularly stained for p65 (pNFκB) or IKKγ (N = 5 donors). pDC > 90% viability within 5 h of treatment. (A) Example of gating for p65 (pNFκB) and pIKKγ with VH treated resting and CpG stimulated pDC. (B) CpG induced intracellular expression of pNFκB was suppressed by THC, JWH-015, and JWH-133. (C) CpG induced intracellular expression of IKKγ was suppressed by THC and both CB2-selective agonists. Asterisks indicate statistically significant differences in p65 and IKKγ phosphorylation compared to VC + CpG (*** = P < .001, ** = P < .01, * = P < .05) using a 1-Way ANOVA with Dunnett’s posttest.