ABSTRACT
There is strong evidence that melatonin possesses immunomodulatory activity. It has been shown that it enhances the immune response, acting as a pro-inflammatory agent. It is suggested that melatonin promotes Th1-mediated immune responses by upregulating IL-12 production by antigen presenting cells. In contrast, it has also been shown that melatonin can inhibit Th1 immunity and instead promote a Th2 response. This discrepancy between different observations of the regulatory activity of melatonin on Th1 immunity encouraged us to further investigate the influence of melatonin and its precursor L-tryptophan on Th1 mediated contact hypersensitivity (CHS). Our results show that both melatonin and L-tryptophan inhibit the inflammatory response associated with CHS. Melatonin inhibited the Th1-dependent immune response by suppressing the production of IFN-gamma and IL-12 by cells in the lymph node. On the other hand treatment with L-tryptophan inhibits CHS without affecting INF-gamma production by Th1 effector cells. Observed suppression of CHS after L-tryptophan treatment is at least partly through the production of the anti-inflammatory cytokine IL-10.
