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

First Author  Usuda H Year  1994
Journal  J Submicrosc Cytol Pathol Volume  26
Issue  1 Pages  111-9
PubMed ID  8149328 Mgi Jnum  J:18828
Mgi Id  MGI:66497 Citation  Usuda H, et al. (1994) Ultrastructure of macrophages and dendritic cells in osteopetrosis (op) mutant mice lacking macrophage colony-stimulating factor (M-CSF/CSF-1) activity. J Submicrosc Cytol Pathol 26(1):111-9
abstractText  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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