临床相关的 GABARAP 缺乏症可减轻硼替佐米诱导的多发性骨髓瘤免疫原性细胞死亡。

IF 6.5 2区医学 Q1 IMMUNOLOGY

Oncoimmunology Pub Date : 2024-05-27 eCollection Date: 2024-01-01 DOI:10.1080/2162402X.2024.2360275

Liwei Zhao, Zhe Shen, Guido Kroemer, Oliver Kepp

引用次数: 0

摘要

最近有研究发现，高风险、低预后的 GABA A 型受体相关蛋白（GABARAP）下调会导致多发性骨髓瘤（MM）细胞自噬和钙网蛋白（CALR）表面暴露缺陷，从而对硼替佐米（bortezomib）产生反应。因此，GABARAP缺陷的MM细胞无法发生免疫性细胞死亡。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Clinically relevant GABARAP deficiency abrogates bortezomib-induced immunogenic cell death in multiple myeloma.

Recently, it was revealed that the high-risk, poor-prognosis downregulation of GABA type A receptor-associated protein (GABARAP) causes a defect in both autophagy and surface exposure of calreticulin (CALR) in multiple myeloma (MM) cells responding to bortezomib. Hence, GABARAP-defective MM cells fail to undergo immunogenic cell death.

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来源期刊

Oncoimmunology ONCOLOGYIMMUNOLOGY-IMMUNOLOGY

CiteScore

12.50

自引率

2.80%

发文量

276

审稿时长

24 weeks

期刊介绍： OncoImmunology is a dynamic, high-profile, open access journal that comprehensively covers tumor immunology and immunotherapy. As cancer immunotherapy advances, OncoImmunology is committed to publishing top-tier research encompassing all facets of basic and applied tumor immunology. The journal covers a wide range of topics, including: -Basic and translational studies in immunology of both solid and hematological malignancies -Inflammation, innate and acquired immune responses against cancer -Mechanisms of cancer immunoediting and immune evasion -Modern immunotherapies, including immunomodulators, immune checkpoint inhibitors, T-cell, NK-cell, and macrophage engagers, and CAR T cells -Immunological effects of conventional anticancer therapies.