Faculty Research 1990 - 1999

Ultrastructure of macrophages and dendritic cells in osteopetrosis (op) mutant mice lacking macrophage colony-stimulating factor (M-CSF/CSF-1) activity.

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Cell-Differentiation: de, Cell-Division: de, Dendritic-Cells: de, ul, Female, Homozygote, Human, Macrophage-Colony-Stimulating-Factor: ge, df, Macrophages: de, ul, Male, Mice, Mice-Inbred-C3H, Mice-Inbred-C57BL, Mice-Mutant-Strains, Microscopy-Electron, Osteopetrosis: dt, ge, pa, Recombinant-Proteins, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S

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J Submicrosc Cytol Pathol 1994 Jan;26(1):111-9




The ultrastructural features of macrophages and dendritic cells of mice homozygous for osteopetrosis (op/op) mutation were studied. The mutant mice are characterized by defective differentiation of osteoclasts, monocytes, and tissue macrophages due to the lack of functional macrophage colony stimulating factor (M-CSF/CSF-1) activity. In op/op mice, tissue macrophages were reduced in number and smaller than in normal littermates. Macrophages in op/op mice showed various degrees of phagocytosis but the development of intracytoplasmic organelles and microvillous projections was poor. After administration of CSF-1 daily for 2 weeks, macrophages in op/op mice developed lysosomes and microvillous projections. In the thymic medulla, T-cell zone of lymph nodes, splenic white pulp and epidermis of the op/op mice, the number of dendritic cells was similar to that in normal littermates and the dendritic cells developed a tubulovesicular system typical of interdigitating cells. Birbeck granules in epidermal Langerhans cells were detected in unmanipulated op/op mice, op/op mice injected with CSF-1, and normal littermates or control mice. However, in untreated op/op mice, dendritic cells projected shorter cytoplasmic processes than in normal littermates, normal control mice and CSF-1 injected op/op mice. These results indicate that the differentiation and maturation of tissue macrophages are mediated by CSF-1, but the dendritic cell differentiation is controlled by other factor(s) than CSF-1, most probably by GM-CSF.

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