Role of macrophage-colony-stimulating factor in regulating the accumulation and phenotype of tumor-associated macrophages
| Autor: | Shona T. Dougherty, G J Dougherty, William H. McBride, Connie J. Eaves |
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| Rok vydání: | 1997 |
| Předmět: |
Macrophage colony-stimulating factor
Cancer Research medicine.medical_treatment Immunology Macrophage-activating factor Mice SCID Biology Mice medicine Animals Immunology and Allergy Macrophage Severe combined immunodeficiency Tumor microenvironment Macrophage Colony-Stimulating Factor Macrophages Cell Differentiation Neoplasms Experimental Macrophage Activation medicine.disease Phenotype Mice Mutant Strains Cytokine Oncology Cell culture Cancer research |
| Zdroj: | Cancer Immunology, Immunotherapy. 44:165-172 |
| ISSN: | 1432-0851 0340-7004 |
| DOI: | 10.1007/s002620050369 |
| Popis: | In order to better define the role played by tumor-cell-derived macrophage-colony-stimulating factor (M-CSF) in regulating the recruitment and phenotype of tumor-associated macrophages, Polyoma large T-transformed fibroblastoid cell lines, derived from M-CSF-deficient osteopetrotic op/op mice and their phenotypically normal op/+ littermate controls, were inoculated into SCID (severe combined immunodeficiency) recipients and both the proportion and phenotype of the macrophages present within the tumors generated were determined. The results obtained indicate that, although tumors derived from M-CSF-deficient and M-CSF-producing tumor cell inoculate contain a similar proportion of macrophages, the macrophages isolated from tumors lacking M-CSF appear morphologically less mature and express lower levels of interleukin 1 beta, tumor necrosis factor alpha and FcR gamma II mRNA. Taken together, these data suggest that, although M-CSF does not appear to play a critical role in determining the macrophage content of these tumors, it does play a role in modulating the phenotype, and potentially the functional activity of the macrophages present within the tumor microenvironment. |
| Databáze: | OpenAIRE |
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