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Myeloid-derived suppressor cells in cancer and cancer therapy
Nature Reviews Clinical Oncology ( IF 78.8 ) Pub Date : 2024-01-08 , DOI: 10.1038/s41571-023-00846-y
Samantha A. Lasser , Feyza G. Ozbay Kurt , Ihor Arkhypov , Jochen Utikal , Viktor Umansky

Anticancer agents continue to dominate the list of newly approved drugs, approximately half of which are immunotherapies. This trend illustrates the considerable promise of cancer treatments that modulate the immune system. However, the immune system is complex and dynamic, and can have both tumour-suppressive and tumour-promoting effects. Understanding the full range of immune modulation in cancer is crucial to identifying more effective treatment strategies. Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population of myeloid cells that develop in association with chronic inflammation, which is a hallmark of cancer. Indeed, MDSCs accumulate in the tumour microenvironment, where they strongly inhibit anticancer functions of T cells and natural killer cells and exert a variety of other tumour-promoting effects. Emerging evidence indicates that MDSCs also contribute to resistance to cancer treatments, particularly immunotherapies. Conversely, treatment approaches designed to eliminate cancer cells can have important additional effects on MDSC function, which can be either positive or negative. In this Review, we discuss the interplay between MDSCs and various other cell types found in tumours as well as the mechanisms by which MDSCs promote tumour progression. We also discuss the relevance and implications of MDSCs for cancer therapy.



中文翻译:

癌症和癌症治疗中的骨髓源性抑制细胞

抗癌药物继续在新批准的药物清单中占据主导地位,其中大约一半是免疫疗法。这一趋势说明了调节免疫系统的癌症治疗的巨大前景。然而,免疫系统是复杂且动态的,可以同时具有抑制肿瘤和促进肿瘤的作用。了解癌症的全方位免疫调节对于确定更有效的治疗策略至关重要。骨髓源性抑制细胞 (MDSC) 是一种异质性骨髓细胞群,与慢性炎症相关,而慢性炎症是癌症的标志。事实上,MDSC 在肿瘤微环境中积累,强烈抑制 T 细胞和自然杀伤细胞的抗癌功能,并发挥多种其他促肿瘤作用。新的证据表明,MDSC 也会导致对癌症治疗(尤其是免疫疗法)的耐药性。相反,旨在消除癌细胞的治疗方法可以对 MDSC 功能产生重要的额外影响,可以是积极的,也可以是消极的。在这篇综述中,我们讨论了 MDSC 与肿瘤中发现的各种其他细胞类型之间的相互作用,以及 MDSC 促进肿瘤进展的机制。我们还讨论了 MDSC 对癌症治疗的相关性和影响。

更新日期:2024-01-09
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