肿瘤细胞治疗研究
英文原题：CX3CL1: a key switch of cell death immunogenicity.
CX3CL1（fractalkine）是一种独特的趋化因子，在癌症生物学中具有双重作用，既能发挥促肿瘤作用，也能发挥抑肿瘤作用。
CX3CL1（fractalkine）是一种独特的趋化因子，在癌症生物学中具有双重作用，既能发挥促肿瘤作用，也能发挥抑肿瘤作用。CX3CL1通过其受体CX3CR1发挥作用，通过招募免疫抑制性髓源性抑制细胞，促进免疫逃逸、血管生成、转移以及肿瘤细胞存活和增殖。相反，它可以通过将细胞毒性T淋巴细胞、NK 细胞和树突状细胞吸引到肿瘤微环境中来增强抗肿瘤免疫。CX3CL1还与促进免疫原性细胞死亡诱导的抗癌免疫反应有关。然而，CX3CL1的过度表达可能 paradoxically 抑制免疫激活，突显了其应用中剂量和背景的重要性。基于CX3CL1的基因或mRNA疗法，特别是与免疫检查点抑制剂联合使用，在癌症治疗中显示出有前景的潜力。
CX3CL1 (fractalkine) is a unique chemokine with dual roles in cancer biology, capable of exerting both tumor-promoting and tumor-suppressive effects. Acting through its receptor CX3CR1, CX3CL1 facilitates immune evasion, angiogenesis, metastasis, and tumor cell survival and proliferation by recruiting immunosuppressive myeloid-derived suppressor cells. Conversely, it can enhance antitumor immunity by attracting cytotoxic T lymphocytes, natural killer cells, and dendritic cells into the tumor microenvironment. CX3CL1 has also been implicated in promoting immunogenic cell death-induced anticancer immune responses. However, excessive expression of CX3CL1 may paradoxically suppress immune activation, highlighting the importance of dose and context in its application. CX3CL1-based gene or mRNA therapies, particularly in combination with immune checkpoint inhibitors, show promising potential for cancer treatment.
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