Abstract
Prostaglandins of the E-series (PGE) have been shown to have numerous effects on the cellular components of the immune system (for review see 1). PGE modulates the cytotoxicity of natural killer (NK) cells (2, 3) and also has been suggested to serve as a negative feedback regulator of macrophage-mediated cytotoxicity (4, 5). Immunoglobulin production by B cells is augmented by PGE (6), whereas blastogenesis of T cells after mitogen stimulation and cell-mediated immunity are inhibited by PGE (7, 8, 9). Growth and differentiation of the granulocyte-macrophage-committed stem cell (GM-CFU-C) in the bone marrow appears to be regulated by the antagonistic effects of colony-stimulating factor and PGE (10). Additionally, PGE production by tumor cells has been suggested to be a mechanism by which tumor cells can escape the host’s immune surveillance (11). The major source for PGE in the immune system has been shown to be monocytes and macrophages (Mø) (12). When stimulated with different agents, such as lipopolysaccharide (LPS) and zymosan, mononuclear phagocytes increase their PGE production and release high amounts of PGE (5, 13, 14). Several biological response modifiers (BRMs) have been reported to be Mø activators and some also augment NK cells (for review see 15). A few have also been shown to activate naive macrophages directly in vitro to express a tumoricidal response. Few studies have been conducted to assess whether BRMs, reported to be Mø activators, could alter PGE production.
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© 1985 Martinus Nijhoff Publishing, Boston
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Chirigos, M.A., Schlick, E., Hartung, K. (1985). Regulation of Prostaglandin Synthesis by Biological Response Modifiers and Effect on Natural Killer Cells and Bone Marrow. In: Goodwin, J.S. (eds) Prostaglandins and Immunity. Prostaglandins, Leukotrienes, and Cancer, vol 4. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2603-8_8
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DOI: https://doi.org/10.1007/978-1-4613-2603-8_8
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