Melatonin enhances Th2 cell mediated immune responses: Lack of sensitivityto reversal by naltrexone or benzodiazepine receptor antagonists

Chronic administration of melatonin for 5 days to antigen-primed mice incre ased the production of pro-inflammatory cytokine IL-10 but decreased the se cretion of anti-inflammatory cytokine TNF-alpha. These results further conf irm that melatonin activates Th2-like immune response. Whether melatonin-me diated Th2 response is dependent on opioid or central and peripheral benzod iazepine receptors was also examined. Hence, melatonin was administered to antigen-sensitised mice with either naltrexone (a mu opioid receptor antago nist) or flumazenil (a central benzodiazepine receptor antagonist) or PK111 95 (a peripheral benzoidiazepine receptor antagonist). No significant diffe rence in melatonin-induced Th2 cell response was observed by naltrexone, fl umazenil or PK11195 treatment. These findings suggest that the Th2 cell res ponse induced by melatonin in antigen sensitised mice neither dependent on endogenous opioid system nor is modulated through the central or peripheral benzodiazepine receptors.