| Autor: |
Konopski, Z., Seljelid, R., Eskeland, T. |
| Předmět: |
|
| Zdroj: |
Scandinavian Journal of Immunology; May1993, Vol. 37 Issue 5, p587-592, 6p |
| Abstrakt: |
Under serum-free conditions the β-glucan receptor of mouse macrophages mediates phagocytosis of β-1,3-D-glucan-coated microbeads (diameter 2 µm). IFN-γ increases the phagocytic function of the β-glucan receptor in a dose-dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN-γ to the cells. The effect disappears within 24 h. The effect of IFN-γ may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis. IL-1 also increases the phagocytic function of the β-glucan receptor giving a dose-dependent response and with the plateau level reached at 10 U/ml. Maximum activity is found 4 h after addition of IL-1 to macrophages. The effect disappears within 24 h. TNF does not alter the phagocytic function of the β-glucan receptor, but TNF together with IL-1 prolongs the effect of IL-1. PGE2 reduces the phagocytic function of the β-glucan receptor. Maximum reduction is achieved with 8 ng/ml. Time-course studies show the lowest phagocytic activity 9 h after addition of PGE2 to the cells. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Plný text