2019 Fiscal Year Research-status Report
The role of LILRB4 on MDSC-mediated immunosuppression in tumor environment
| Project/Area Number |
19K16705
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| Research Institution | Tohoku University |
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Principal Investigator |
蘇 美慈 東北大学, 加齢医学研究所, 助教 (00812116)
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| Project Period (FY) |
2019-04-01 – 2022-03-31
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| Keywords | MDSC / LILRB4 / tumor metastasis / immunosuppression / gp49B |
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| Outline of Annual Research Achievements |
Myeloid-derived suppressor cells (MDSCs) regulate tumor-associated immunosuppression, and the polarization of MDSCs can dominate tumor progression. In this study, we demonstrated that the immunoglobulin-like receptor subfamily B member 4 (LILRB4) orchestrates MDSCs polarization to exhibit M2 activated phenotype. Knockout of LILRB4 promoted macrophage secreted anti-tumor cytokines and inhibited migration of tumor cells. Deficiency of murine gp49B, the ortholog of LILRB4, reduced tumor-infiltrating MDSCs and inhibited tumor angiogenesis. In addition, Lewis lung carcinoma (LLC) cells- and B16F10 melanoma cells-mediated tumor metastases were reduced in gp49B deficient mice. Here we suggest that LILRB4 may serves as a target for blocking of MDSC-mediated immunosuppression.
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| Current Status of Research Progress |
Current Status of Research Progress
2: Research has progressed on the whole more than it was originally planned.
Reason
The experiments were carried our according to our expectations, and the experimental results also supported our hypothesis.
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| Strategy for Future Research Activity |
We need to further investigate the detailed mechanism of LILRB4-mediated tumor suppression in tumor environment. For therapeutic applications, the strategies for targeting LILRB4 (gp49B) in tumor-bearing mice will be studied.
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