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Phagocytic efficacy of macrophage‐like cells as a function of cell cycle and Fcγ receptors (FcγR) and complement receptor (CR)3 expression
Author(s) -
Luo Y.,
Cook E.,
Fries B. C.,
Casadevall A.
Publication year - 2006
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2006.03132.x
Subject(s) - phagocytosis , receptor expression , complement receptor , microbiology and biotechnology , biology , receptor , cell cycle , macrophage , cell , cell sorting , fc receptor , opsonin , flow cytometry , immunology , complement system , antibody , biochemistry , in vitro
Summary Previous studies have shown that the efficiency of phagocytosis is a function of cell cycle and that phagocytosis promotes cell cycle progression. Because phagocytosis is dependent on cellular receptors we hypothesized that Fcγ receptors (FcγR) and complement receptors (CR) expression varied with cell cycle. Consequently, we used centrifugal elutriation of macrophage‐like cells, fluorescence activated cell sorting analysis and receptor staining to investigate expression of FcγR and CR as a function of cell cycle. We confirmed that FcγR expression on macrophage‐like cells increased as the cells progressed from G1 to G2 phases. Moreover, CR3 expression varied as a function of cell cycle in a manner similar to FcγR. Correlation of receptor expression with cell size showed that FcγR and CR3 expression on macrophages was determined largely by cell size enlargement during the cell cycle. The efficacy of both Fc‐ and complement‐mediated phagocytosis of live Cryptococcus neoformans (Cn) showed a biphasic pattern with the efficacy of phagocytosis decreasing when the cells approached the G1–S interface, which paralleled the changes in receptor surface expression when cells exited G1 phase. Live Cn cells were significantly more resistant to phagocytosis than dead cells at all stages of macrophage‐like cell cycle. In contrast to live cells, the efficacy of phagocytosis of dead Cn decreased as surface receptor expression increased. Hence, the efficacy of phagocytosis in this system as function of cell cycle is not related to phagocytic receptor expression.

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