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Differentiation of Cell Surface Receptors on Normal Human Bone Marrow Myeloid Precursors
Author(s) -
Barrett Sondra G.,
Hansen Keith S.,
Bainton Dorothy F.
Publication year - 1981
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1981.tb02741.x
Subject(s) - receptor , myeloid , promyelocyte , cell surface receptor , complement receptor , biology , microbiology and biotechnology , fc receptor , bone marrow , cell , immunology , complement system , chemistry , antibody , biochemistry
S ummary. Receptors for IgG and complement are present on the plasma membrane of functionally mature blood neutrophils. Neutrophilic precursors lack these membrane receptors, which may account for their diminished phagocytic capability. In this study, myeloid precursors from human bone marrow were examined for the presence and activity of membrane receptors for IgG and activated complement. Morphologic identification by light microscopy of neutrophilic cells was made by rosetting techniques and chloroacetate esterase cytochemical staining and at the ultrastructural level by peroxidase reactivity. This study showed that the Fc receptor was the only membrane marker on the myeloblast and that the number of cells with this receptor increased with maturation. Functional investigation of the Fc receptor indicated that its presence on early myeloid cells was insufficient to induce IgG‐mediated ingestion. Phagocytosis via the Fc receptor was not acquired until the metamyelocyte stage. Complement receptors, C3d and C3b, appeared later than the Fc receptor. The C3d receptor, detected first on the promyelocyte, remained relatively constant throughout maturation, whereas the C3b receptor acquired at the myelocyte stage increased with maturation. These data provide evidence that distinct membrane changes occur during normal myeloid cell maturation and that the presence of these membrane receptors is not sufficient for Fc‐mediated ingestion to occur.