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. Author manuscript; available in PMC: 2010 Apr 16.
Published in final edited form as: J Neuroimmune Pharmacol. 2009 Mar 3;4(2):249–259. doi: 10.1007/s11481-009-9148-4

Fig. 3.

Fig. 3

Differentiation of DC in the presence of the CB2 receptor agonist O-1966 affects their capacity to stimulate T cell proliferation and the cytokine/chemokine profile. a Bone marrow-derived DC from C57BL/6 (H-2b) mice were differentiated in the presence or absence of 10−7 M O-1966 (DCCB2 or DC) for 7 days. Different numbers of purified CD11c+ DCCB2 or DC were co-cultured with purified CD4+ T cells from B10. A mice (H-2k) (1×106 cells/ml) for 4 days. Proliferation was determined by BrdU incorporation. Controls included T cells alone, DC or DCCB2 alone. b DCCB2 or DC (2.5×105 cells/ml) were co-cultured with CD4+ T cells (1×106 cells/ml) for 48 h. Culture supernatants were tested for cytokine/chemokine release by Bioplex technology. c DCCB2 were generated in the presence of various O-1966 concentrations (10−7, 10−8, and 10−9 M) and co-cultured with allogeneic T cells for 48 h. IFNγ and IL-17 secretion was determined by ELISA