Regulation of NKG2D Stress Ligands and Its Relevance in Cancer Progression.
Regulation of NKG2D Stress Ligands and Its Relevance in Cancer Progression.
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细胞应激期间的免疫监视是维持体内平衡所必需的。在受损细胞中，应激（自然杀伤组2成员D (NKG2D)）配体的表达被诱导到细胞上，以促进细胞毒性免疫群体的识别。这一过程体现在癌症的发生、发展和维持过程中。不幸的是，癌细胞的适应产生了多种机制来逃避免疫细胞的识别。因此，人们已经进行了广泛的研究，以诱导肿瘤细胞上的应激配体来补充免疫治疗的努力。在这篇综述中，我们提供了当前涉及应激配体诱导和抑制的调控机制的最新进展，并提供了该主题研究进展的考虑领域。在细胞窘迫下，正常稳态信号的多个方面被改变或破坏。在免疫环境中，外部和内部应激源通常会促进自然杀伤组2成员D （NKG2D）配体的表达，从而允许NKG2D受体承载效应群体靶向识别和杀死细胞。NKG2D配体的存在或缺失会严重影响疾病进展并影响免疫治疗选择的可及性。在癌症中，已知肿瘤细胞对与肿瘤进展和维持直接相关的NKG2D配体具有不同的调节机制。因此，了解NKG2D配体在癌症中的调控将允许靶向治疗努力，旨在利用应激反应途径。在这篇综述中，我们总结了目前对NKG2D配体在癌症中诱导和抑制的调控机制的理解。此外，我们强调了目前针对NKG2D配体表达的治疗努力，并提供了我们对进一步加强NKG2D配体生物学领域的考虑的观点。
Immune surveillance during periods of cellular stress is necessary to maintain homeostasis. In distressed cells, the expression of stress (natural killer group 2 member D (NKG2D)) ligands is induced on cells to promote recognition by cytotoxic immune populations. This process is exemplified during cancer initiation, progression, and maintenance. Unfortunately, cancer cell adaptation yields multiple mechanisms to evade immune cell recognition. Therefore, extensive efforts have been investigated to induce stress ligands on tumor cells to complement immunotherapy efforts. In this review, we provide updates on the current regulatory mechanisms involved with both stress ligand induction and repression and offer areas of consideration as research on this topic progresses. Under cellular distress, multiple facets of normal homeostatic signaling are altered or disrupted. In the context of the immune landscape, external and internal stressors normally promote the expression of natural killer group 2 member D (NKG2D) ligands that allow for the targeted recognition and killing of cells by NKG2D receptor-bearing effector populations. The presence or absence of NKG2D ligands can heavily influence disease progression and impact the accessibility of immunotherapy options. In cancer, tumor cells are known to have distinct regulatory mechanisms for NKG2D ligands that are directly associated with tumor progression and maintenance. Therefore, understanding the regulation of NKG2D ligands in cancer will allow for targeted therapeutic endeavors aimed at exploiting the stress response pathway. In this review, we summarize the current understanding of regulatory mechanisms controlling the induction and repression of NKG2D ligands in cancer. Additionally, we highlight current therapeutic endeavors targeting NKG2D ligand expression and offer our perspective on considerations to further enhance the field of NKG2D ligand biology.
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影响因子：
11.2
作者：
Ashiru O;Boutet P;Fernández-Messina L;Agüera-González S;Skepper JN;Valés-Gómez M;Reyburn HT
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Reyburn HT
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7.3
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影响因子：
56.9
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Bauer, S;Groh, V;Spies, T
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影响因子：
3.2
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7.2
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