CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题：Targeting NKG2D/NKG2DL axis in multiple myeloma therapy.
Targeting NKG2D/NKG2DL axis in multiple myeloma therapy.
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多发性骨髓瘤（MM）患者的免疫效应细胞处于许多免疫治疗的前沿，目前已开发出多种方法来充分利用免疫细胞的抗肿瘤潜力。T细胞和NK细胞来源的免疫淋巴细胞均表达活化性NK受体NKG2D。该受体可识别八种不同的NKG2D配体（NKG2DL），包括主要组织相容性复合体I类（MHC）链相关蛋白A和B（MICA和MICB）。它们与NKG2D的结合触发T细胞和NK细胞的效应功能。NKG2DL在MM细胞中具有多态性。NKG2DL在细胞表面表达降低可通过多种肿瘤免疫逃逸机制来解释。在这篇综述中，我们讨论了NKG2D/NKG2DL轴调控免疫效应细胞的机制，以及在多发性骨髓瘤中促进NKG2DL表达并抑制其释放的策略，并提出在MM细胞中增加NKG2DL表达同时增强NK细胞活化和杀伤功能的治疗策略。
Immune effector cells in patients with multiple myeloma (MM) are at the forefront of many immunotherapy treatments, and several methods have been developed to fully utilise the antitumour potential of immune cells. T and NK cell-derived immune lymphocytes both expressed activating NK receptor group 2 member D(NKG2D). This receptor can identify eight distinct NKG2D ligands (NKG2DL), including major histocompatibility complex class I (MHC) chain-related protein A and B (MICA and MICB). Their binding to NKG2D triggers effector roles in T and NK cells.
NKG2DL is polymorphic in MM cells. The decreased expression of NKG2DL on the cell surface is explained by multiple mechanisms of tumour immune escape. In this review, we discuss the mechanisms by which the NKG2D/NKG2DL axis regulates immune effector cells and strategies for promoting NKG2DL expression and inhibiting its release in multiple myeloma and propose therapeutic strategies that increase the expression of NKG2DL in MM cells while enhancing the activation and killing function of NK cells.
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