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肝内区域免疫对肝移植后肿瘤复发的影响 Review
刘江, 卢宠茂, 万钧
《工程（英文）》 2022年 第10卷 第3期 页码 57-64 doi: 10.1016/j.eng.2021.11.012
免疫调节细胞生物学及其在急性移植物抗宿主病预防或治疗中的临床应用 Review
Bruce R. Blazar
《工程（英文）》 2019年 第5卷 第1期 页码 98-105 doi: 10.1016/j.eng.2018.11.016
关键词： 移植物抗宿主病（GVHD） 免疫调节细胞 细胞疗法
免疫抑制和肝移植 Review
Jan Lerut, Samuele Iesari
《工程（英文）》 2023年 第21卷 第2期 页码 175-187 doi: 10.1016/j.eng.2022.07.007
完美的手术技术和充分的免疫抑制是确保最佳移植物和患者存活的关键。不同药物的可用性导致了一些通常由行业驱动的不同类型的临床试验，以寻找理想的免疫抑制方案。然而，大量概念不同的研究设计未能明确定义最佳免疫抑制方案。基于钙调神经磷酸酶抑制剂他克莫司、抗代谢药物霉酚酸酯或硫唑嘌呤和短期类固醇（除了可能的诱导外）的三联免疫抑制方案仍然是目前公认的肝移植标准免疫抑制方案。然而，鉴于排斥定义的变化、免疫抑制负荷的定制以及由于慢性免疫抑制引起的长期副作用，未来的试验最好包括一个以上的终点，而不是急性T细胞介导的急性排斥（a-TCMR）或肾衰竭。这些免疫现象应根据一系列长期的生物学和组织学随访进行检查。临床相关α-TCMR的诊断和治疗应基于综合生物学、免疫学和组织病理学的发现。
免疫细胞在器官移植免疫排斥和免疫耐受中的不同作用 Review
干晓杰, 古鉴, 鞠峥, 吕凌
《工程（英文）》 2022年 第10卷 第3期 页码 44-56 doi: 10.1016/j.eng.2021.03.029
器官移植免疫排斥反应是由多种细胞参与的复杂的免疫应答过程，是决定移植成败和患者生存的关键因素。目前大多数器官移植患者采用免疫抑制剂和生物制剂的组合疗法来控制移植器官的免疫排斥反应，然而免疫抑制剂的使用会降低移植患者免疫系统功能，导致严重的并发症，如慢性感染、恶性肿瘤等。因
此，彻底了解器官移植免疫耐受和免疫排斥的相关机制对于开发更好的治疗方案和改善患者预后至关重要。本文对免疫细胞在器官移植免疫排斥和免疫耐受诱导过程中的作用，以及目前针对移植患者处于临床试验阶段的新型细胞治疗进行概述。
质谱流式技术在脑免疫研究中的应用 Review
王艳, Baohui Xu, 薛丽香
《工程（英文）》 2022年 第16卷 第9期 页码 187-197 doi: 10.1016/j.eng.2021.06.022
杨建宁,孙玉坤,李自成,孙运全
《中国工程科学》 2007年 第9卷 第10期 页码 30-35
针对高维非线性电力系统复杂的控制对象，在静止无功发生器（SVG）的电压偏差-无功的控制方法上，采用人体免疫系统维持自身功能正常的机理，以稳定电力系统工作状态,提出基于人工免疫算法的SVG外环控制器控制策略。结果表明，所提出的仿生免疫机理的控制方案对于SVG中动态无功调节过程和对电力系统稳定性的控制作用是有效的。
基于自然杀伤细胞的癌症免疫疗法的进展和前景 Review
胡渊, 田志刚, 张彩
《工程（英文）》 2019年 第5卷 第1期 页码 106-114 doi: 10.1016/j.eng.2018.11.015
自然杀伤（natural killer，NK）细胞是重要的先天免疫细胞，位于机体抵御病毒感染和癌症的第一道防线。这些策略包括：上调自然杀伤细胞抑制性受体的配体，产生可溶性分子或免疫抑制因子。文中总结了肿瘤逃逸自然杀伤细胞识别的机制、自然杀伤细胞免疫疗法的现状和进展、提升自然杀伤细胞体内抗肿瘤能力的途径以及该领域在临床实践中所面临的重大挑战。
基于转录组学及多尺度生物测定多模态鉴定宣肺败毒方抑制巨噬细胞免疫反应的活性成分 Article
赵璐, 刘豪, 王迎超, 王书芳, 荀得金, 王毅, 程翼宇, 张伯礼
《工程（英文）》 2023年 第20卷 第1期 页码 63-76 doi: 10.1016/j.eng.2021.09.007
131I标记的人源化抗B7-H3抗体用于胶质母细胞瘤放射免疫疗法的治疗特性 Article
, Meng Zheng, Shandong Zhao, Yan Wang, Minzhou Huang, Hanqing Chen, Ziyi Huang, Kaijie Zhang, 缪丽燕, 张学光
《工程（英文）》 2023年 第30卷 第11期 页码 190-202 doi: 10.1016/j.eng.2023.05.011
B7 homolog 3 (B7-H3) has attracted much attention in glioblastoma (GBM) radioimmunotherapy (RIT) due to its abnormally high expression on tumor cells. In this study, we report that two specific humanized anti-human B7-H3 antibodies (hu4G4 and hu4H12) derived from mouse anti-human B7-H3 antibodies that were generated by computer-aided design and exclusively recognize membrane expression of B7-H3 by human glioma cells. Hu4G4 and hu4H12 were radiolabeled with 89Zr for RIT antibody screening. Micro-positron emission tomography (PET) imaging, biodistribution and pharmacokinetic (PK) analyses of 89Zr-labeled antibodies were performed in U87-xenografted models. 125I labelling of the antibodies for single-photon emission computed tomography (SPECT) imaging was also used to investigate the biological behavior of the antibodies in vivo. Furthermore, the pharmacodynamic (PD) of the 131Ilabeled antibodies were evaluated in U87-xenografted mice and GL261 Red-FLuc-B7-H3 in situ glioma tumor models. Micro-PET imaging and biodistribution analysis with a gamma counter showed that 89Zr-deferoxamine (DFO)-hu4G4 had higher tumor targeting performance with lower liver uptake than 89Zr-DFO (hu4H12, immunoglobulin G (IgG)). The biodistribution results of 125I-SPECT imaging were similar to those of 89Zr-PET imaging, though the biodistribution in long bone joints and the thyroid varied. The PD analysis results indicated that 131I-hu4G4 had an excellent therapeutic effect and high safety with no apparent toxicity. Interestingly, 131I-hu4G4 improved the tumor vasculature in tissues with higher expression of collagen type IV and platelet-derived growth factor receptor b (PDGFR-b) compared with control treatment, as determined by immunofluorescence (IF), which contributed to inhibiting tumor growth. Taken together, our data indicate that hu4G4 exhibits good tumor targeting and specificity, achieves low nonspecific concentrations in normal tissues, and has acceptable PK characteristics. 131I-hu4G4 also exerts effective antitumor effects with an ideal safety profile. Therefore, we expect hu4G4 to be an excellent antibody for the development of GBM RIT.
关键词： B7-H3 Radioimmunotherapy Glioblastoma Pharmacokinetics Pharmacodynamics
代谢组扩展生物学的“旁中心法则”——对理解基因组学-糖组学-代谢组学-表观基因组学互作的意义
Albert Stuart Reece
《工程（英文）》 2023年 第26卷 第7期 页码 16-16 doi: 10.1016/j.eng.2022.07.011
The central dogma of biology holds that the transcription of DNA into RNA and the translation of RNA into proteins forms the primary axis of biological activity [1]. Following major advances in the description of the complex glycan and lipid chains that are added onto these basic building blocks, the glycome and lipidome have recently been added to this doctrine as an exciting new extension named the ‘‘paracentral dogma” [2]. However, it has been pointed out that biological systems can include many layers, which are described in modern omics technology platforms relating to both cell-intrinsic and cell-extrinsic layers of control, including metabolomic, microbiomic, immunological, epigenomic, epitranscriptomic, proteomic and phosphoproteomic layers [3].
It is well known that stem and progenitor cells have a metabolism that is based on glycolysis and glutaminolysis [4]. Although this provides less energy to the cell than oxidative phosphorylation, it suffices for these cells’ needs, since such cells are generally relatively quiescent and normally suppress energy-intensive processes such as genome duplication and transcription. Moreover, it has been shown that the high intracellular lactate levels involved in such states not only inhibits the key gatekeeper enzymes of oxidative phosphorylation (i.e., pyruvate dehydrogenase and carnitine palmitoyl acyltransferase) but also actually covalently modifies them by lactylation in order to maintain this inhibited metabolic–epigenomic state [5]. In addition, intermediate metabolism and nutrients are the source of the very extensive library of post-translational modifications to DNA, RNA, and proteins, as well as supplying cellular energy for many of the required reactions. Hence, the metabolic state locks in and reinforces the epigenomic state, and the metabolome and epigenome thereby play mutually reinforcing roles. This self-reinforcing coordination explains why it is so difficult to generate induced pluripotent cells and is a contributory explanation for why the described protocols typically have such low cellular yields.
These concepts become even more important when it is considered that cancer cells are de-differentiated, similarly rely on glycolysis and glutaminolysis, and are similarly metabolically–epigenomically–genomically synchronized. The disruption of this metabolic system is a key focus of mechanistic cancer research.
These important considerations imply that the descriptive and predictive power of the newly described ‘‘paracentral dogma” of biology may be usefully and meaningfully extended by including the metabolome, along with the genome, transcriptome, proteome, glycome, and lipidome, to describe cell-intrinsic regulation—not only in terms of another omics analytical layer but also as a fully predictive and interactive partner in the symphonic-like multilayer coordination that evidently comprises cellular regulatory layering.
调节性T细胞及其在抗肿瘤免疫疗法中的临床应用 Review
解丰, 梁瑞, 李丹, 李斌
《工程（英文）》 2019年 第5卷 第1期 页码 132-139 doi: 10.1016/j.eng.2018.12.002
标题 作者 时间 类型 操作
131I标记的人源化抗B7-H3抗体用于胶质母细胞瘤放射免疫疗法的治疗特性
, Meng Zheng, Shandong Zhao, Yan Wang, Minzhou Huang, Hanqing Chen, Ziyi Huang, Kaijie Zhang, 缪丽燕, 张学光
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