Raghavendra, V and Singh, V and Shaji, A V and Vohra, H and Kulkarni, S K and Agrewala, J N (2001) Melatonin provides signal 3 to unprimed CD4(+) T cells but failed to stimulate LPS primed B cells. Clinical and experimental immunology, 124 (3). pp. 414-22. ISSN 0009-9104
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Abstract
Growing evidence has supported the conclusion that melatonin, a pineal hormone, modulates the immune function. In our previous study, we evaluated in vivo the potential role of melatonin in the regulation of the antigen specific T and B cells. In the present study, we observe that melatonin down-regulated the expression of the co-stimulatory molecule B7-1 but not B7-2 on macrophages. Further, melatonin encouraged the proliferation of anti-CD3 antibody activated CD4(+) T cells only in the presence of antigen-presenting cells and promoted the production of Th2-like cytokines. Furthermore, it failed to influence the activity of B cells in a T-independent manner. Melatonin suppressed the release of TNF-alpha by LPS or IFN-gamma activated macrophages 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.
Item Type: | Article |
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Additional Information: | Copyright of this article belongs to Wiley. |
Uncontrolled Keywords: | B cells and macrophages;CD4+ T cells;melatonin;unprimed Th1 and Th2 cells |
Subjects: | Q Science > QR Microbiology > QR180 Immunology |
Depositing User: | Dr. K.P.S.Sengar |
Date Deposited: | 03 Feb 2012 16:15 |
Last Modified: | 03 Feb 2012 16:15 |
URI: | http://crdd.osdd.net/open/id/eprint/864 |
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