2017 Fiscal Year Final Research Report
Study for mechanism of STING-mediated inflammation in tumor microenvironment
| Project/Area Number |
16K19070
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Human pathology
|
|---|
| Research Institution | Asahikawa Medical College |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Keywords | STING / macrophages |
|---|
| Outline of Final Research Achievements |
STING contributes to anti-tumor immunity through sensing tumor-derived genomic DNAs in the tumor-bearing host. Although injection of STING ligands into tumor sites shows anti-tumor effects via inducing type I IFNs and activating immune system, precise events caused in the tumor remain to be assessed. We found that CD11b+ Ly6C+ cells were found to robustly accumulate into the tumor site after intratumoral injection of STING ligand, cGAMP in the 4T1 mouse model. The accumulating subsets were positive for F4/80 and Ly6C but not Ly6G, macrophage phenotypes. The accumulating macrophages in the tumor site were also confirmed in the other mouse models. In STING-deficient mice, intratumoral cGAMP treatment did not induce macrophage accumulation. The functional analyses revealed that the macrophages showed activities of phagocytosis and TNFa production. These results demonstrate that the accumulating macrophages into the tumor site by STING stimulation contribute to the anti-tumor immunity.
|
| Free Research Field |
tumor immunology, pathology
|
