| 研究実績の概要 |
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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