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Scand J Immunol. 1993 May;37(5):587-92.

Cytokines and PGE2 modulate the phagocytic function of the beta-glucan receptor in macrophages.

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1
Department of Experimental Pathology and Anatomy, Institute of Medical Biology, University of Tromsø, Norway.

Abstract

Under serum-free conditions the beta-glucan receptor of mouse macrophages mediates phagocytosis of beta-1,3-D-glucan-coated microbeads (diameter 2 microns). IFN-gamma increases the phagocytic function of the beta-glucan receptor in a dose-dependent manner, giving the plateau level at 100 U/ml. Maximum activity appears 9 h after addition of IFN-gamma to the cells. The effect disappears within 24 h. The effect of IFN-gamma may be a result of augmented receptor synthesis since treatment with cycloheximide reduces the phagocytosis. IL-1 also increases the phagocytic function of the beta-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 beta-glucan receptor, but TNF together with IL-1 prolongs the effect of IL-1. PGE2 reduces the phagocytic function of the beta-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.

[Indexed for MEDLINE]

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