CB2

Cannabinoid receptor CB2 (CB2R) is a cannabinoid G protein-coupled receptor originally characterized as a peripheral receptor expressed in macrophages and immune tissues^[1][2]. Mechanistically, CB2R couples through Gi/o proteins, inhibits adenylyl cyclase, and activates MAPK signaling, linking cannabinoid receptor signaling to immune-cell regulation^[3]. In inflammatory biology, CB2R modulates immune-cell functions in cell systems and animal models, and CB2-deficient mice show exacerbated inflammatory phenotypes^[2]. In neuroinflammation, CB2R activity is especially relevant in macrophage-lineage cells and CNS microglia, connecting peripheral immune regulation with central immune responses^[4]. Compared with CB1, CB2 is distinguished by immune-enriched distribution, while CB1 is found predominantly in neuronal tissues and also couples to ion-channel signaling^[5]. For experimental applications, CB2-selective agonists such as HU-308 bind CB2 efficiently, inhibit forskolin-stimulated cyclic AMP production in CB2-transfected cells, and support receptor-selective studies of inflammation and peripheral analgesia^[6].- CB2R links cannabinoid receptor signaling with immune modulation, inflammation models, and neuroimmune research design^[2][4]. - CB2 differs from CB1 mainly by immune distribution, not by complete separation of signaling pathways^[5]. - HU-308 supports CB2-selective pharmacology studies in inflammation, peripheral analgesia, and cAMP assays^[6].