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Macrophage migration inhibitor factor (MIF): Potential role in cognitive impairment disorders 巨噬细胞迁移抑制因子 (MIF):在认知障碍疾病中的潜在作用
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.03.003
Lian Zeng , Pengchao Hu , Yu Zhang , Mingyue Li , Yilin Zhao , Shiyong Li , Ailin Luo

Macrophage migration inhibitory factor (MIF) is a cytokine in the immune system, participated in both innate and adaptive immune responses. Except from immune cells, MIF is also secreted by a variety of non-immune cells, including hematopoietic cells, endothelial cells (ECs), and neurons. MIF plays a crucial role in various diseases, such as sepsis, rheumatoid arthritis, acute kidney injury, and neurodegenerative diseases. The role of MIF in the neuropathogenesis of cognitive impairment disorders is emphasized, as it recruits multiple inflammatory mediators, leading to activating microglia or astrocyte-derived neuroinflammation. Furthermore, it contributes to the cell death of neurons and ECs with the binding of apoptosis-inducing factor (AIF) through parthanatos-associated apoptosis-inducing factor nuclease (PAAN) / MIF pathway. This review comprehensively delves into the relationship between MIF and the neuropathogenesis of cognitive impairment disorders, providing a series of emerging MIF-targeted pharmaceuticals as potential treatments for cognitive impairment disorders.

巨噬细胞迁移抑制因子(MIF)是免疫系统中的一种细胞因子,参与先天性和适应性免疫反应。除免疫细胞外,多种非免疫细胞也会分泌 MIF,包括造血细胞、内皮细胞(EC)和神经元。MIF 在败血症、类风湿性关节炎、急性肾损伤和神经退行性疾病等多种疾病中发挥着重要作用。MIF 在认知障碍疾病的神经发病机制中的作用得到了强调,因为它能招募多种炎症介质,导致激活小胶质细胞或星形胶质细胞衍生的神经炎症。此外,它还会通过parthanatos-associated apoptosis-inducing factor nuclease (PAAN) / MIF途径与凋亡诱导因子(AIF)结合,导致神经元和EC的细胞死亡。本综述全面探讨了 MIF 与认知障碍疾病的神经发病机制之间的关系,并提供了一系列新兴的 MIF 靶向药物,作为认知障碍疾病的潜在治疗方法。
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引用次数: 0
From orphan to oncogene: The role of GPR35 in cancer and immune modulation 从孤儿到癌基因:GPR35 在癌症和免疫调节中的作用。
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.03.004
Simran Takkar , Gunjan Sharma , Jyoti B. Kaushal , K.M. Abdullah , Surinder K. Batra , Jawed A. Siddiqui

G protein-coupled receptors (GPCRs) are well-studied and the most traceable cell surface receptors for drug discovery. One of the intriguing members of this family is G protein-coupled receptors 35 (GPR35), which belongs to the class A rhodopsin-like family of GPCRs identified over two decades ago. GPR35 presents interesting features such as ubiquitous expression and distinct isoforms. Moreover, functional and genome-wide association studies on its widespread expression have linked GPR35 with pathophysiological disease progression. Various pieces of evidence have been accumulated regarding the independent or endogenous ligand-dependent role of GPR35 in cancer progression and metastasis. In the current scenario, the relationship of this versatile receptor and its putative endogenous ligands for the activation of oncogenic signal transduction pathways at the cellular level is an active area of research. These intriguing features offered by GPR35 make it an oncological target, justifying its uniqueness at the physiological and pathophysiological levels concerning other GPCRs. For pharmacologically targeting receptor-induced signaling, few potential competitive antagonists have been discovered that offer high selectivity at a human level. In addition to its fascinating features, targeting GPR35 at rodent and human orthologue levels is distinct, thus contributing to the sub-species selectivity. Strategies to modulate these issues will help us understand and truly target GPR35 at the therapeutic level. In this article, we have provided prospects on each topic mentioned above and suggestions to overcome the challenges. This review discusses the molecular mechanism and signal transduction pathways activated by endogenous ligands or spontaneous auto-activation of GPR35 that contributes towards disease progression. Furthermore, we have highlighted the GPR35 structure, ubiquitous expression, its role in immunomodulation, and at the pathophysiological level, especially in cancer, indicating its status as a versatile receptor. Subsequently, we discussed the various proposed ligands and their mechanism of interaction with GPR35. Additionally, we have summarized the GPR35 antagonist that provides insights into the opportunities for therapeutically targeting this receptor.

G 蛋白偶联受体(GPCR)是研究得最透彻的细胞表面受体,也是药物发现中最容易追踪的细胞表面受体。二十多年前发现的 G 蛋白偶联受体 35(GPR35)属于 GPCR 的 A 类视黄醛样家族,是这一家族中引人入胜的成员之一。GPR35 具有无处不在的表达和不同的同工型等有趣特征。此外,对其广泛表达的功能性和全基因组关联研究表明,GPR35 与病理生理疾病的进展有关。关于 GPR35 在癌症进展和转移中的独立或内源性配体依赖性作用,已经积累了各种证据。在目前的情况下,这种多用途受体及其假定的内源性配体在细胞水平激活致癌信号转导通路的关系是一个活跃的研究领域。GPR35 所具有的这些引人入胜的特点使其成为肿瘤靶点,并证明了它在生理和病理生理学水平上相对于其他 GPCR 的独特性。在以受体诱导信号为药物靶点方面,已发现的潜在竞争性拮抗剂中,只有少数能在人体水平上提供高选择性。除了其引人入胜的特点外,靶向啮齿动物和人类同源物水平的 GPR35 也各不相同,因此造成了亚种选择性。调节这些问题的策略将有助于我们了解并真正在治疗层面上靶向 GPR35。在本文中,我们对上述每个主题进行了展望,并提出了克服挑战的建议。本综述讨论了由内源性配体激活或 GPR35 自发自动激活导致疾病进展的分子机制和信号转导途径。此外,我们还强调了 GPR35 的结构、泛在表达、在免疫调节中的作用以及在病理生理学水平上的作用,尤其是在癌症中的作用,这表明它是一种多功能受体。随后,我们讨论了各种拟议配体及其与 GPR35 的相互作用机制。此外,我们还总结了 GPR35 拮抗剂,为针对该受体的治疗提供了机会。
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引用次数: 0
Exogenous drug-induced mouse models of atopic dermatitis 外源性药物诱导的特应性皮炎小鼠模型
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.01.003
Rou Zheng , Yan Ren , Xinyue Liu , Canxia He , Hua Liu , Yixuan Wang , Jianing Li , Shuya Xia , Zhifang Liu , Yizhao Ma , Dianchen Wang , Suling Xu , Geng Wang , Na Li

Atopic dermatitis (AD) is an inflammatory skin disease characterized by intense pruritus. AD is harmful to both children and adults, but its pathogenic mechanism has yet to be fully elucidated. The development of mouse models for AD has greatly contributed to its study and treatment. Among these models, the exogenous drug-induced mouse model has shown promising results and significant advantages. Until now, a large amount of AD-related research has utilized exogenous drug-induced mouse models, leading to notable advancements in research. This indicates the crucial significance of applying such models in AD research. These models exhibit diverse characteristics and are highly complex. They involve the use of various strains of mice, diverse types of inducers, and different modeling effects. However, there is currently a lack of comprehensive comparative studies on exogenous drug-induced AD mouse models, which hinders researchers' ability to choose among these models. This paper provides a comprehensive review of the features and mechanisms associated with various exogenous drug-induced mouse models, including the important role of each cytokine in AD development. It aims to assist researchers in quickly understanding models and selecting the most suitable one for further investigation.

特应性皮炎(AD)是一种以剧烈瘙痒为特征的炎症性皮肤病。特应性皮炎对儿童和成人都有害,但其致病机制尚未完全阐明。小鼠皮炎模型的开发极大地促进了皮炎的研究和治疗。在这些模型中,外源性药物诱导小鼠模型显示出了良好的效果和显著的优势。迄今为止,大量与阿德相关的研究都采用了外源性药物诱导小鼠模型,从而取得了显著的研究进展。这表明将此类模型应用于注意力缺失症研究具有至关重要的意义。这些模型表现出多种多样的特点,而且非常复杂。它们涉及使用不同品系的小鼠、不同类型的诱导剂和不同的建模效果。然而,目前缺乏关于外源性药物诱导的 AD 小鼠模型的全面比较研究,这阻碍了研究人员在这些模型中进行选择。本文全面综述了各种外源性药物诱导的小鼠模型的特点和相关机制,包括每种细胞因子在AD发展过程中的重要作用。它旨在帮助研究人员快速了解模型,并选择最合适的模型进行进一步研究。
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引用次数: 0
Corrigendum to “Immune evasion of neutralizing antibodies by SARS-CoV-2 Omicron” [Cytokine Growth Factor Rev. 70 (2023) 13–25] 对 "SARS-CoV-2 Omicron 对中和抗体的免疫逃避 "的更正 [Cytokine Growth Factor Rev. 70 (2023) 13-25].
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.03.006
Lidong Wang , Michelle Møhlenberg , Pengfei Wang , Hao Zhou
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引用次数: 0
Z-DNA binding protein 1 orchestrates innate immunity and inflammatory cell death Z-DNA 结合蛋白 1 协调先天免疫和炎症细胞死亡。
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.03.005
Qixiang Song , Yuhang Fan , Huali Zhang , Nian Wang

Innate immunity is not only the first line of host defense against microbial infections but is also crucial for the host responses against a variety of noxious stimuli. Z-DNA binding protein 1 (ZBP1) is a cytosolic nucleic acid sensor that can induce inflammatory cell death in both immune and nonimmune cells upon sensing of incursive virus-derived Z-form nucleic acids and self-nucleic acids via its Zα domain. Mechanistically, aberrantly expressed or activated ZBP1 induced by pathogens or noxious stimuli enables recruitment of TANK binding kinase 1 (TBK1), interferon regulatory factor 3 (IRF3), receptor-interacting serine/threonine-protein kinase 1 (RIPK1) and RIPK3 to drive type I interferon (IFN-I) responses and activation of nuclear factor kappa B (NF-κB) signaling. Meanwhile, ZBP1 promotes the assembly of ZBP1- and absent in melanoma 2 (AIM2)-PANoptosome, which ultimately triggers PANoptosis through caspase 3-mediated apoptosis, mixed lineage kinase domain like pseudokinase (MLKL)-mediated necroptosis, and gasdermin D (GSDMD)-mediated pyroptosis. In response to damaged mitochondrial DNA, ZBP1 can interact with cyclic GMP-AMP synthase to augment IFN-I responses but inhibits toll like receptor 9-mediated inflammatory responses. This review summarizes the structure and expression pattern of ZBP1, discusses its roles in human diseases through immune-dependent (e.g., the production of IFN-I and pro-inflammatory cytokines) and -independent (e.g., the activation of cell death) functions, and highlights the attractive prospect of manipulating ZBP1 as a promising therapeutic target in diseases.

先天免疫不仅是宿主抵御微生物感染的第一道防线,而且对于宿主应对各种有害刺激也至关重要。Z-DNA 结合蛋白 1(ZBP1)是一种细胞膜核酸传感器,可通过其 Zα 结构域感知入侵病毒衍生的 Z 型核酸和自身核酸,从而诱导免疫细胞和非免疫细胞的炎性细胞死亡。从机理上讲,病原体或有害刺激诱导异常表达或活化的 ZBP1 可招募 TANK 结合激酶 1(TBK1)、干扰素调节因子 3(IRF3)、受体丝氨酸/苏氨酸蛋白激酶 1(RIPK1)和 RIPK3,以驱动 I 型干扰素(IFN-I)反应和激活核因子卡巴 B(NF-κB)信号。同时,ZBP1 促进 ZBP1- 和缺失黑色素瘤 2(AIM2)-PANoptosome 的组装,最终通过 caspase 3 介导的细胞凋亡、混合系激酶域类伪激酶(MLKL)介导的坏死和 gasdermin D(GSDMD)介导的热凋亡触发 PANoptosis。针对受损的线粒体 DNA,ZBP1 可与环 GMP-AMP 合成酶相互作用,增强 IFN-I 反应,但抑制收费类受体 9 介导的炎症反应。这篇综述总结了 ZBP1 的结构和表达模式,讨论了它通过免疫依赖性(如产生 IFN-I 和促炎细胞因子)和非依赖性(如激活细胞死亡)功能在人类疾病中的作用,并强调了操纵 ZBP1 作为疾病治疗靶点的诱人前景。
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引用次数: 0
When pyro(ptosis) meets palm(itoylation) 当 "火烧"(ptosis)遇到 "棕榈"(itoylation)
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.03.001
Lu Jiang , Zirui Wang , Ting Xu , Leiliang Zhang

Pyroptosis, a programmed cell death process, is vital for the immune response against microbial infections and internal danger signals. Recent studies have highlighted the importance of protein palmitoylation, a modification that involves attaching palmitate to cysteine residues, in regulating key proteins involved in pyroptosis. Palmitoylation of cGAS at residue C474 by ZDHHC18 affects its enzymatic activity and DNA binding ability. Similarly, ZDHHC9 promotes cGAS activity through palmitoylation at residues C404/405. NLRP3 palmitoylation at residue C844, mediated by ZDHHC12, impacts its stability and interactions with other proteins, crucial for activating the NLRP3 inflammasome and triggering inflammation. However, the role of ZDHHC5 in NLRP3 palmitoylation remains uncertain due to conflicting findings. Palmitoylation at C88/91 is essential for STING activation and induction of type I interferons. It modulates the formation of multimeric complexes and downstream signaling pathways. GSDMD palmitoylation at C191 is necessary for pore formation and membrane translocation, while GSDME palmitoylation at C407/408 is associated with drug-induced pyroptosis. Moreover, palmitoylation of NOD1 and NOD2 influences their membrane recruitment and immune signaling pathways in response to bacterial peptidoglycans, acting as upstream regulators of pyroptosis. This review summarizes the important roles for palmitoylation in regulating the function of key pyroptosis-related proteins, shedding light on the intricate mechanisms governing immune responses and inflammation.

细胞热解是一种程序性细胞死亡过程,对于针对微生物感染和内部危险信号的免疫反应至关重要。最近的研究强调了蛋白质棕榈酰化(一种将棕榈酸连接到半胱氨酸残基上的修饰)在调节参与裂解过程的关键蛋白质中的重要性。ZDHHC18 对 cGAS 的残基 C474 进行棕榈酰化会影响其酶活性和 DNA 结合能力。同样,ZDHHC9 通过残基 C404/405 的棕榈酰化作用促进 cGAS 的活性。由 ZDHHC12 介导的 NLRP3 在残基 C844 处的棕榈酰化会影响其稳定性以及与其他蛋白质的相互作用,这对激活 NLRP3 炎症小体和引发炎症至关重要。然而,ZDHHC5 在 NLRP3 棕榈酰化中的作用仍不确定,因为研究结果相互矛盾。C88/91 处的棕榈酰化对 STING 的激活和 I 型干扰素的诱导至关重要。它能调节多聚复合物的形成和下游信号通路。GSDMD 在 C191 处的棕榈酰化是孔形成和膜转运的必要条件,而 GSDME 在 C407/408 处的棕榈酰化与药物诱导的热变态反应有关。此外,NOD1 和 NOD2 的棕榈酰化会影响它们对细菌肽聚糖的膜招募和免疫信号通路,成为热蛋白沉积的上游调节因子。这篇综述总结了棕榈酰化在调节关键的热渗透相关蛋白功能方面的重要作用,揭示了支配免疫反应和炎症的复杂机制。
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引用次数: 0
Glycosylation of FGF/FGFR: An underrated sweet code regulating cellular signaling programs 成纤维细胞生长因子/成纤维细胞生长因子受体的糖基化:调节细胞信号程序的甜蜜密码。
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.04.001
Aleksandra Gędaj, Paulina Gregorczyk, Dominika Żukowska, Aleksandra Chorążewska, Krzysztof Ciura, Marta Kalka, Natalia Porębska, Łukasz Opaliński

Fibroblast growth factors (FGFs) and their receptors (FGFRs) constitute plasma-membrane localized signaling hubs that transmit signals from the extracellular environment to the cell interior, governing pivotal cellular processes like motility, metabolism, differentiation, division and death. FGF/FGFR signaling is critical for human body development and homeostasis; dysregulation of FGF/FGFR units is observed in numerous developmental diseases and in about 10% of human cancers. Glycosylation is a highly abundant posttranslational modification that is critical for physiological and pathological functions of the cell. Glycosylation is also very common within FGF/FGFR signaling hubs. Vast majority of FGFs (15 out of 22 members) are N-glycosylated and few FGFs are O-glycosylated. Glycosylation is even more abundant within FGFRs; all FGFRs are heavily N-glycosylated in numerous positions within their extracellular domains. A growing number of studies points on the multiple roles of glycosylation in fine-tuning FGF/FGFR signaling. Glycosylation modifies secretion of FGFs, determines their stability and affects interaction with FGFRs and co-receptors. Glycosylation of FGFRs determines their intracellular sorting, constitutes autoinhibitory mechanism within FGFRs and adjusts FGF and co-receptor recognition. Sugar chains attached to FGFs and FGFRs constitute also a form of code that is differentially decrypted by extracellular lectins, galectins, which transform FGF/FGFR signaling at multiple levels. This review focuses on the identified functions of glycosylation within FGFs and FGFRs and discusses their relevance for the cell physiology in health and disease.

成纤维细胞生长因子(FGFs)及其受体(FGFRs)是质膜定位的信号枢纽,可将信号从细胞外环境传递到细胞内部,从而控制细胞的运动、新陈代谢、分化、分裂和死亡等关键过程。成纤维细胞生长因子/成纤维细胞生长因子受体信号转导对人体发育和稳态至关重要;在许多发育疾病和约 10% 的人类癌症中都可观察到成纤维细胞生长因子/成纤维细胞生长因子受体单元失调的现象。糖基化是一种高度丰富的翻译后修饰,对细胞的生理和病理功能至关重要。糖基化在 FGF/FGFR 信号转导枢纽中也非常常见。绝大多数 FGF(22 个成员中的 15 个)都是 N-糖基化的,只有少数 FGF 是 O-糖基化的。糖基化在表皮生长因子受体(FGFRs)中更为丰富;所有表皮生长因子受体在其细胞外结构域的许多位置都有大量的 N-糖基化。越来越多的研究指出了糖基化在微调表皮生长因子/表皮生长因子受体信号转导中的多重作用。糖基化改变了表皮生长因子的分泌,决定了其稳定性,并影响其与表皮生长因子受体和共受体的相互作用。表皮生长因子受体的糖基化决定了其在细胞内的排序,在表皮生长因子受体内构成自抑机制,并调整表皮生长因子和共受体的识别。附着在表皮生长因子和表皮生长因子受体上的糖链还构成了一种密码形式,细胞外凝集素(galectins)可对其进行不同程度的解密,从而在多个层面上改变表皮生长因子/表皮生长因子受体的信号转导。这篇综述将重点讨论在 FGFs 和 FGFRs 中已确定的糖基化功能,并讨论它们与健康和疾病中的细胞生理学的相关性。
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引用次数: 0
Interleukins and interferons in mesenchymal stromal stem cell-based gene therapy of cancer 白细胞介素和干扰素在基于间充质基质干细胞的癌症基因疗法中的应用。
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.03.002
Urban Švajger , Urška Kamenšek

The tumor microenvironment is importantly shaped by various cytokines, where interleukins (ILs) and interferons (IFNs) shape the balance of immune activity within tumor niche and associated lymphoid organs. Their importance in activation and tuning of both innate and adaptive immune responses prompted their use in several clinical trials, albeit with limited therapeutic efficacy and risk of toxicity due to systemic administration. Increasing preclinical evidence suggests that local delivery of ILs and IFNs could significantly increase their effectiveness, while simultaneously attenuate the known side effects and issues related to their biological activity. A prominent way to achieve this is to use cell-based delivery vehicles. For this purpose, mesenchymal stromal stem cells (MSCs) are considered an almost ideal candidate. Namely, MSCs can be obtained in large quantities and from obtainable sources (e.g. umbilical cord or adipose tissue), their ex vivo expansion is relatively straightforward compared to other cell types and they possess very low immunogenicity making them suitable for allogeneic use. Importantly, MSCs have shown an intrinsic capacity to respond to tumor-directed chemotaxis. This review provides a focused and detailed discussion on MSC-based gene therapy using ILs and IFNs, engineering techniques and insights on potential future advancements.

各种细胞因子对肿瘤微环境起着重要作用,其中白细胞介素(ILs)和干扰素(IFNs)决定着肿瘤龛和相关淋巴器官内免疫活动的平衡。白细胞介素和干扰素在激活和调整先天性免疫反应和适应性免疫反应方面具有重要作用,这促使它们被用于多项临床试验,尽管疗效有限,而且由于全身给药还存在毒性风险。越来越多的临床前证据表明,ILs 和 IFNs 的局部给药可以显著提高它们的疗效,同时减轻已知的副作用和与它们的生物活性有关的问题。实现这一目标的一个重要方法是使用基于细胞的递送载体。为此,间充质基质干细胞(MSCs)被认为是几乎理想的候选者。也就是说,间充质干细胞可以从可获得的来源(如脐带或脂肪组织)中大量获得,与其他细胞类型相比,间充质干细胞的体外扩增相对简单,而且间充质干细胞的免疫原性很低,适合异体使用。重要的是,间充质干细胞具有对肿瘤引导的趋化做出反应的内在能力。本综述重点详细讨论了使用 ILs 和 IFNs 的间充质干细胞基因疗法、工程技术以及对未来潜在进展的见解。
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引用次数: 0
Unveiling the role of IL-17: Therapeutic insights and cardiovascular implications 揭示 IL-17 的作用:治疗见解和对心血管的影响。
IF 9.3 2区 医学 Q1 Medicine Pub Date : 2024-06-01 DOI: 10.1016/j.cytogfr.2024.05.001
Kexin Jiang , Yanjiani Xu , Yan Wang , Nanhao Yin , Fangyang Huang , Mao Chen

Interleukin-17 (IL-17), a pivotal cytokine in immune regulation, has attracted significant attention in recent years due to its roles in various physiological and pathological processes. This review explores IL-17 in immunological context, emphasizing its structure, production, and signaling pathways. Specifically, we explore its involvement in inflammatory diseases and autoimmune diseases, with a notable focus on its emerging implications in cardiovascular system. Through an array of research insights, IL-17 displays multifaceted functions yet awaiting comprehensive discovery. Highlighting therapeutic avenues, we scrutinize the efficacy and clinical application of four marketed IL-17 mAbs along other targeted therapies, emphasizing their potential in immune-mediated disease management. Additionally, we discussed the novel IL-17D-CD93 axis, elucidating recent breakthroughs in their biological function and clinical implications, inviting prospects for transformative advancements in immunology and beyond.

白细胞介素-17(IL-17)是一种在免疫调节中起关键作用的细胞因子,近年来因其在各种生理和病理过程中的作用而备受关注。这篇综述探讨了免疫学背景下的 IL-17,强调了它的结构、产生和信号传导途径。具体而言,我们探讨了 IL-17 在炎症性疾病和自身免疫性疾病中的参与,并重点关注其在心血管系统中的新影响。通过一系列的研究发现,IL-17 具有多方面的功能,但尚待全面发掘。为了突出治疗途径,我们仔细研究了四种已上市的 IL-17 mAbs 及其他靶向疗法的疗效和临床应用,强调了它们在免疫介导疾病治疗中的潜力。此外,我们还讨论了新型 IL-17D-CD93 轴,阐明了它们在生物功能和临床影响方面的最新突破,为免疫学及其他领域的变革性进展提供了前景。
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引用次数: 0
Cytokines and soluble mediators as architects of tumor microenvironment reprogramming in cancer therapy 细胞因子和可溶性介质是癌症治疗中肿瘤微环境重编程的设计师
IF 13 2区 医学 Q1 Medicine Pub Date : 2024-02-28 DOI: 10.1016/j.cytogfr.2024.02.003
Suling Xu , Qingqing Wang , Wenxue Ma

Navigating the intricate landscape of the tumor microenvironment (TME) unveils a pivotal arena for cancer therapeutics, where cytokines and soluble mediators emerge as double-edged swords in the fight against cancer. This review ventures beyond traditional perspectives, illuminating the nuanced interplay of these elements as both allies and adversaries in cancer dynamics. It critically evaluates the evolving paradigms of TME reprogramming, spotlighting innovative strategies that target the sophisticated network of cytokines and mediators. Special focus is placed on unveiling the therapeutic potential of novel cytokines and mediators, particularly their synergistic interactions with extracellular vesicles, which represent underexplored conduits for therapeutic targeting. Addressing a significant gap in current research, we explore the untapped potential of these biochemical players in orchestrating immune responses, tumor proliferation, and metastasis. The review advocates for a paradigm shift towards exploiting these dynamic interactions within the TME, aiming to transcend conventional treatments and pave the way for a new era of precision oncology. Through a critical synthesis of recent advancements, we highlight the imperative for innovative approaches that harness the full spectrum of cytokine and mediator activities, setting the stage for breakthrough therapies that offer heightened specificity, reduced toxicity, and improved patient outcomes.

在错综复杂的肿瘤微环境(TME)中,细胞因子和可溶性介质成为抗击癌症的双刃剑。这篇综述超越了传统视角,揭示了这些元素在癌症动力学中既是盟友又是对手的微妙相互作用。它批判性地评估了TME重编程不断演变的范例,重点介绍了针对细胞因子和介质复杂网络的创新策略。文章特别关注揭示新型细胞因子和介质的治疗潜力,尤其是它们与细胞外囊泡之间的协同作用,因为细胞外囊泡是尚未充分开发的治疗靶向渠道。针对当前研究中存在的重大空白,我们探讨了这些生化角色在协调免疫反应、肿瘤增殖和转移方面尚未开发的潜力。这篇综述倡导范式转变,利用肿瘤组织器官内的这些动态相互作用,旨在超越传统治疗方法,为精准肿瘤学的新时代铺平道路。通过对最新进展的批判性综述,我们强调了利用细胞因子和介质的全方位活动的创新方法的必要性,为提高特异性、降低毒性和改善患者预后的突破性疗法奠定了基础。
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引用次数: 0
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Cytokine & Growth Factor Reviews
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