cause a stimulating effect. For example, it was found that in vivo and in vitro treatment of rats with peritoneal macrophages CP55940 leads to a reduced migration in vitro to the peptide methionyl leucine phenylalanine formal in a mode of Haupts Is chlich CB2 Reported similar. FMLP to the chemotactic response CAL-101 GS-1101 of mouse macrophages has also been shown to be reduced by cannabidiol, a cannabinoid Of these, weakly to CB2. A link to CB2 was involved in this reaction because of the CB2-selective antagonist SR144528 prevented the decrease in migration. Was observed in contrast to events for DC-9-THC, it was found that two AG trigger migration of microglia and CB2 is involved in this effect.
Recently, in studies that a pharmacological approach, together with a genetic approach that mice macrophages employees knockout M, Has been shown to inhibit DC-9-THC and CP55940 chemotaxis of peritoneal macrophages of the mouse RANTES used / CCL5 in a mode that CB2 has been linked. You -9 THC and CP55940 BI 2536 disabling reactive Ability to migrate to the chemokine RANTES or CCL5, an event that is obtained by activation of G-protein-coupled chemokine receptor CCR5 Ltlichen the group, suggested that CB2 signaling leads to crosstalk between these receptor and CCR5. Thus, these and other studies in which the CB2 Including transductional as an essential element of a network of systems G-protein coupled receptor signal peptide Lich chemokine receptors that act in a coordinated manner, modulating macrophage migration. It has also been shown that CB2 cannabinoid-in-mediated inhibition is involved Processing of antigens by macrophages.
In studies conducted to investigate the effect of DC-9-THC in the treatment of intact lysozyme by macrophages, it was shown that DC-9-THC, the F ability A macrophage reduces hybridoma to act as an antigen-pr Sentierende cell based on their R ability, secrete IL-2 after stimulation of an l soluble protein antigen-specific helper T-cell hybridoma. DC-9-THC exposure setting Born a significant reduction in T-cell response to the native form of lysozyme after pretreatment of macrophages with nanomolar drug. However, SR-9 THC no effect on IL-2 production when the macrophages pr A synthetic peptide antigen will present on T cells, suggesting that the drug with antigen processing and Pr Presentation of non-disabled peptides .
The inhibition of cannabinoid The T-cell response to native lysozyme stereoselective, in accordance with the inclusion of a cannabinoid receptor Of bioactive CP55940 in the activation of T cells from, w n During the relatively inactive stereoisomer CP56667 has not done so. The macrophage hybridoma expressed mRNA for CB2, but not CB1. Otherwise have the selective CB1 antagonist SR141716A does not cause against the suppression of DC-9 THC, w completely While the CB2 selective antagonist SR144528 YOUR BIDDING blocked the suppression of SR-9 THC in the cellular T. Together these provide Ren answer results macrophages as the target of inhibition of cannabinoid Processing of the antigen in a manner which was operatively connected to CB2. Clinical implications and applications cannabinoid The ligands that signal through cannabinoid receptors Of particularly useful as a means can be for therapeutic manipulation of hyperinflammatory immune responses in the CNS. These compounds are highly lipophilic and easily penetrate the BBB in this context, a Cabral and Thomas Griffin Expert Rev Mol Med page 11 Aut