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Phagocytosis by Receptors for C3b (CR 1 ), iC3b (CR 3 ), and IgG (Fc) on Human Peritoneal Macrophages
Author(s) -
Newman Simon L.,
Becker Susanne,
Halme Jouko
Publication year - 1985
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.38.2.267
Subject(s) - phagocytosis , receptor , fc receptor , biology , complement receptor , ic3b , macrophage , monocyte , antibody , microbiology and biotechnology , complement system , in vitro , immunology , biochemistry
Human peritoneal macrophages (HPM) obtained via laparoscopy were examined for the presence and functional capacity of complement and Fc receptors. Between 5 and 20 ml of peritoneal fluid containing 1–2 × 10 6 macrophages/ml was available for each study. Macrophages made up 80–95% of the cells in the fluid. Fc and C3 receptors on HPM were characterized by rosette formation with, and phagocytosis of, IgG‐ and C3‐coated sheep erythrocytes (E). EIgG were bound by 82% and ingested by 63% of HPM, with 4–15 E ingested/HPM. The HPM formed rosettes with EC3b (56%) and EC3bi (71%) but not EC3d,g or EC3d. Antibodies to complement receptors type 1 (CR 1 ) and type 3 (CR 3 ) inhibited rosette formation with EC3b and EC3bi, respectively, indicating that HPM possessed separate and distinct receptors for the C3b and iC3b ligands. In 60% of the samples studied, HPM demonstrated the ability to ingest both EC3b and EC3bi, as well as ElgG. Because of the heterogeneous nature of the cells obtained in peritoneal fluid, due to their progressive change from monocytelike cells into mature macrophages, HPM were separated by 1 g velocity sedimentation into fractions of increasing maturity. They were then examined for phagocytosis via Fc and complement receptors. Fc receptor mediated phagocytosis occurred throughout the monocyte‐to‐macrophage maturation sequence, while the ability of HPM to ingest via CR 1 and CR 3 was maturation dependent, with ingestion via CR 3 occurring before CR 1 , in a manner analogous to in vitro differentiation of monocyte‐derived macrophages.