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• W2021072785 abstract "Abstract Despite reports on the secretion of granulocyte — macrophage — colony‐stimulating factor (GM‐CSF) by murine peritoneal macrophages in response to inflammatory stimuli, the ability of human monocytes to generate this growth factor has remained doubtful. Neither endotoxin, phorbol compounds, nor inflammatory cytokines have been shown to elicit GM‐CSF by these cells. Our present studies indicate that exposure of monocytes to solid‐phase murine IgG 2a , but not to murine IgG 1 and thus cross‐linkage of the 72‐kDa FcγRI results in transcription of the GM‐CSF gene, accumulation of stable GM‐CSF mRNA and finally in release of biologically active GM‐CSF protein. Cross‐linking of FcγRI by a murine anti‐FcγRI monoclonal antibody and goat anti‐mouse antibody failed, however, to stimulate GM‐CSF release. This suggests that high affinity Fc‐FcγRI interactions are required for induction of expression of GM‐CSF by monocytes." @default.
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• W2021072785 date "1992-07-01" @default.
• W2021072785 modified "2023-09-27" @default.
• W2021072785 title "Secretion of granulocyte-macrophage colony-stimulating factor by human blood monocytes is stimulated by engagement of Fcγ receptors type I by solid-phase immunoglobulins requiring high-affinity Fc-Fcγ receptor type I interactions" @default.
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• W2021072785 doi "https://doi.org/10.1002/eji.1830220703" @default.
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• W2021072785 hasPublicationYear "1992" @default.
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