Melatonin provides signal 3 to unprimed CD4(+) T cells but failed to stimulate LPS primed B cells

Growing evidence has supported the conclusion that melatonin, a pineal horm one, modulates the immune function. In our previous study, we evaluated in vivo the potential role of melatonin in the regulation of the antigen speci fic T and B cells. In the present study, we observe that melatonin down-reg ulated the expression of the co-stimulatory molecule B7-1 but not B7-2 on m acrophages. Further, melatonin encouraged the proliferation of anti-CD3 ant ibody activated CD4(+) T cells only in the presence of antigen-presenting c ells and promoted the production of Th2-like cytokines. Furthermore, it fai led to influence the activity of B cells in a T-independent manner. Melaton in suppressed the release of TNF-alpha by LPS or IFN-gamma activated macrop hages but failed to inhibit nitric oxide (NO) release. Thus the study shows that melatonin can engineer the growth of unprimed CD4(+) T cells if both the signals are provided by antigen-presenting cells. However, it could not regulate the function of B cells.