Abstract: |
The effect of murine rTNF-α on the binding of human 125I-rCSF-1 to murine thioglycolate-elicited peritoneal exudate macrophages (PEM) was investigated. At 4°C, 125I-CSF-1 binding to PEM was inhibited by preincubation with human rCSF-1, but not by other cytokines. When PEM were incubated with various cytokines at 37°C, murine rTNF-α caused >90% decrease in 125I-CSF-1 binding. This decrease was time, temperature and TNF dose dependent, and was not affected by preincubation with cycloheximide. The reduction in CSF-1-binding activity was reversed by prolonged incubation at 37°C even in the presence of TNF. However, PEM preincubated with TNF subsequently washing free of residual TNF resulted in a rapid recovery of CSF-1 binding. This recovery of CSF-1 binding activity required protein synthesis. Binding studies suggested that the decrease in 125I-CSF-1 binding was most likely caused by a reduction in the number of CSF-1 receptors. In addition, preincubation with TNF at 37°C inhibited 125I-CSF-1 binding on mononuclear phagocytes, including the macrophage cell line J774, bone marrow-derived macrophages, and nonelicited macrophages from three different strains of mice. In contrast, 125I-murine rTNF-α binding to PEM was not inhibited by preincubation with CSF-1 at 4°C or 37°C. These data suggest that TNF may play a role in the modulation of receptor expression on blood cells, and may point to a role for this pleiotropic cytokine in the regulation of hemopoiesis. |
Keywords: |
nonhuman; animal cell; mouse; animal; cytology; mice; biological model; animal experiment; mice, inbred balb c; cytokine; kinetics; cell culture; iodine radioisotopes; recombinant proteins; histochemistry; hematopoiesis; temperature; macrophage; macrophages; colony-stimulating factors; swine; ascitic fluid; tumor necrosis factor; receptors, cell surface; interleukin-1; receptors, tumor necrosis factor; mice, inbred c3h; growth substances; lymphotoxin; granulocyte-macrophage colony-stimulating factor; macrophage activation; cycloheximide; cell receptor; colony stimulating factor; priority journal; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; receptors, colony-stimulating factor
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