期刊
CANCER SCIENCE
卷 100, 期 11, 页码 2160-2166出版社
WILEY
DOI: 10.1111/j.1349-7006.2009.01296.x
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类别
资金
- Ministry of Education, Culture, Sports, Science, and Technology of Japan. [1320390113, 21790388]
- Grants-in-Aid for Scientific Research [21591668, 21790388] Funding Source: KAKEN
Class A scavenger receptors (SR-A, CD204) are highly expressed in tumor-associated macrophages (TAM). To investigate the function of SR-A in TAM, wild-type and SR-A-deficient (SR-A-/-) mice were injected with EL4 cells. Although these groups of mice did not differ in the numbers of infiltrating macrophages and lymphocytes and in neovascularization, SR-A-/- mice had delayed growth of EL4 tumors. Expression of inducible nitric oxide (NO) synthase and interferon (IFN)-gamma mRNA increased significantly in tumor tissues from SR-A-/- mice. Engulfment of necrotic EL4 cells induced upregulation of NO and IFN-gamma production by cultured macrophages, and production of NO and IFN-gamma increased in SR-A-/- macrophages in vitro. IFN-beta production by cultured macrophages was also elevated in SR-A-/- macrophages in vitro. These results suggested that the antitumor activity of macrophages increased in SR-A-/- mice because of upregulation of NO and IFN-gamma production. These data indicate an important role of SR-A in regulating TAM function by inhibiting toll-like receptor (TLR)4-IFN-beta signaling. (Cancer Sci 2009); 00: 000-000).
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