Melatonin inhibits apoptosis during early B-cell development in mouse bone marrow

The pineal secretory product, melatonin, exerts a variety of effects on the immune system. Administration of melatonin stimulates cell‐mediated immunity, particularly by inhibiting apoptosis among T lymphocytes in the thymus and inducing production of T‐cell‐derived cytokines. However, its possible...

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Veröffentlicht in:Journal of pineal research 2000-09, Vol.29 (2), p.86-93
Hauptverfasser: Yu, Qingnan, Miller, Sandra C., Osmond, Dennis G.
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Sprache:eng
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Zusammenfassung:The pineal secretory product, melatonin, exerts a variety of effects on the immune system. Administration of melatonin stimulates cell‐mediated immunity, particularly by inhibiting apoptosis among T lymphocytes in the thymus and inducing production of T‐cell‐derived cytokines. However, its possible effects on the humoral immune system are unclear. In the present study, we have examined whether melatonin may influence the in vivo development of B lymphocytes in mouse bone marrow, a process in which apoptosis is normally a prominent feature. Double immunofluorescence labeling and flow cytometry were used to quantitate phenotypically defined precursor B‐cell and mature B‐cell populations and their apoptotic rates in bone marrow of mice fed either melatonin‐containing or control diet for 16 days from 9 wk of age. In short‐term bone marrow cultures, the incidence of apoptosis among large pre‐B cells, including cells expressing the Λ5 component of pre‐B‐cell receptor, was markedly reduced in melatonin‐treated mice, associated with an increase in the absolute number of large pre‐B cells in bone marrow. In contrast, apoptosis of earlier precursor B cells and mature B lymphocytes did not differ from control values. The results indicate that orally administered melatonin can substantially promote the survival of precursor B cells in mouse bone marrow. Melatonin treatment may thus boost the survival of newly formed B cells mediating humoral immunity.
ISSN:0742-3098
1600-079X
DOI:10.1034/j.1600-079X.2000.290204.x