| Autor: |
Konopski, Z., Seljelid, R., Eskeland, T. |
| Předmět: |
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| Zdroj: |
Scandinavian Journal of Immunology; Jul1994, Vol. 40 Issue 1, p57-63, 7p, 5 Graphs |
| Abstrakt: |
We have previously shown that soluble aminated β-1,3-D-glucan (AG) and glucan-derivatized microbeads (GDM) bind to the specific β-glucan receptor on mouse peritoneal macrophages. Phagocytosis of GDM by macrophages is mediated through the β-glucan receptor. IFN-γ which increases macrophage phagocytic capacity, also increased the phagocytosis of GDM. In the present study we show that IFN-γ inhibits internalization of AG in macrophages in a dose- and time-dependent manner. The inhibitory effect of IFN-γ was neutralized by treatment of the macrophages with cycloheximide. These results were confirmed by confocal laser scanning microscopy which showed that IFN-γ treated cells incorporated less fluorescein-labelled AG than did untreated cells. IFN-γ did not change the macrophage-binding capacity for AG showing that the inhibitory effect of IFN-γ is not caused by decreased number of β-glucan receptors on the cells. The stimulatory effect of AG on IL-1β and TNF-α release from macrophages was reduced by pretreatment of the cells with IFN-γ. We conclude that the uptake of AG and GDM in macrophages, both mediated through the β-glucan receptor, are differently regulated by IFN-γ. The reduced internalization of AG after IFN-γ treatment of macrophages, is probably responsible for the down-regulation of IL-1 and TNF-α secretion. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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