The CD300ld Receptor on Pathologically Activated Neutrophils is Requiredfor Tumor-Driven Immune Suppression
WANG Chaoxiong, ZHENG Peixuan, ZHAO Yun*
Targeting immune checkpoint proteins to enhance the cytotoxic ability of immune effector cellsrepresents a breakthrough in cancer therapy and has achieved promising results in clinical treatments. However, asignificant proportion of cancer patients do not respond to existing immune checkpoint inhibitor therapy due to thehighly immunosuppressive tumor microenvironment. This microenvironment is heterogeneous, and myeloid cellsplay a key role in its establishment, particularly pathologically activated neutrophil, also known as PMN-MDSC(polymorphonuclear myeloid-derived suppressive cell), which is recognized as the major immune suppressor. Unlike normal neutrophils, PMN-MDSC has a strong suppressive ability to lymphocytes. Therefore, identifying specific and effective targets to block PMN-MDSC in the tumor microenvironment is an important avenue of immunotherapy research. This article summarizes the team’s discovery of the membrane protein CD300ld expressed onPMN-MDSC involved in tumor development, and describes in detail the signal transduction mechanism by whichCD300ld functions through downstream S100A8/A9. Targeting CD300ld may potentially become a promising tumor treatment approach, providing new insights for subsequent immunotherapy.
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