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Inhibition of CFU‐E Colony Formation by Resident Peritoneal Macrophages From Hybrids of BALB/c Mice
Author(s) -
Johnson Candace S.,
Furmanski Philip
Publication year - 1984
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.36.5.581
Subject(s) - biology , erythropoiesis , in vitro , macrophage , balb/c , microbiology and biotechnology , erythropoietin , immunology , inbred strain , andrology , biochemistry , immune system , endocrinology , medicine , gene , anemia
In previous studies, macrophages have been shown to influence in vitro colony formation by erythroid progenitors (CFU‐E). To determine whether the origin of the macrophages influences their effects on in vitro erythropoiesis, plasma clot cultures of CFU‐E were grown over adherent monolayers of macrophages from various strains of mice. Macrophages were separated from the plasma clot cultures by an intermediary layer of agar. Normal resident macrophages from BALB/c mice and several other inbred strains had no effect on CFU‐E colony formation. In contrast, macrophages from a strain of mice termed BWF, which were originally identified as BALB/c but subsequently shown to be a hybrid of BALB/c and outbred CFW mice, strongly inhibited erythroid colony formation. Resident macrophages from the parental outbred CFW mice inhibited CFU‐E in 50% of the animals tested. Inhibition was obtained in both homologous and autologous macrophage‐CFU‐E combinations and was therefore not due to histoincompatibility effects, nor was inhibition related to prostaglandin production by the macrophages or to effects on erythropoietin levels in the assay system. The results demonstrate that normal resident macrophages influence in vitro erythropoiesis and that the effects observed are dependent on the genotype of the mice from which the cells are derived.

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