摘要
结缔组织增生对于免疫抵抗性恶性肿瘤的发展、进展和治疗至关重要。针对结缔组织增生相关的代谢途径似乎是一种有趣的方法来扩大我们的一次性抗肿瘤药物的库存。 CXCL12/CXCR4 轴抑制可减少纤维化,减轻免疫抑制并显着提高 PD-1 免疫疗法的疗效。 CD40L 替代疗法可能会增加 T 细胞的活性,下调 CD40+,延长患者的生存期并防止癌症进展。尽管在临床前模型中使用的 FAPα 拮抗剂并未导致永久治愈,但观察到免疫抵抗的减轻、结缔组织的改变和血管生成的减少。靶向 DDR2 可能会增强抗 PD-1 治疗在多种肿瘤细胞系中的效果,并有能力克服黑色素瘤对 BRAF 靶向治疗的适应。重编程结缔组织增生不仅可能与目前的治疗合作,而且可能与其他潜在的治疗靶点合作。我们提出了与结缔组织形成相关的最有希望的代谢途径,并讨论了提高免疫疗法疗效的新兴策略
关键词: 癌症、免疫疗法、结缔组织增生、免疫抗性、CXCR-4、PD-L1。
图形摘要
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