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I don't know about you, but I'm feeling IL-22. 我不知道你怎么想,但我感觉到了 IL-22。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-08 DOI: 10.1016/j.cytogfr.2024.11.001
Logan S Dean, Alissa N Threatt, Kaylee Jones, Emmanuel O Oyewole, Morgan Pauly, Maëlis Wahl, Melea Barahona, Rose W Reiter, Tara M Nordgren

Defense of the human body against damaging and pathogenic insults is a heavily regulated affair. A primary mechanism of defense at sites of insult are soluble mediators whose defensive maneuvers increase barrier integrity and promote pro-reparative and resolution processes. IL-22 is a cytokine in the IL-10 cytokine family that has garnered increased attention in recent years due to its intimate link in promoting resolution of inflammatory insults, while simultaneously being over expressed in certain fibrotic and chronic inflammatory-skewed diseases. The spatial action of IL-22 centers around the barrier sites of the body, including the skin, lungs, and gut mucosa. As such, a detailed understanding of the role of this cytokine, the producers and responders, and the diseases resulting from over- or under-expression have prominent impacts on a variety of disease outcomes. Herein we present a comprehensive review of IL-22; from historical perspectives and initial discovery, as well as more recent data that dramatically expands on the cellular sources and impact of this cytokine. We aim to showcase the duality of IL-22 and highlight addressable gaps in the field of IL-22 crosstalk and impacts at the ever-important mucosal and tissue barrier sites.

人体对破坏性和致病性损伤的防御是一个受到严格调控的过程。受损部位的主要防御机制是可溶性介质,其防御作用可提高屏障的完整性,促进恢复和修复过程。IL-22是IL-10细胞因子家族中的一种细胞因子,由于其与促进炎症损伤的恢复密切相关,同时在某些纤维化和慢性炎症倾斜性疾病中过度表达,因此近年来受到越来越多的关注。IL-22 的作用空间集中在人体的屏障部位,包括皮肤、肺部和肠道粘膜。因此,详细了解这种细胞因子的作用、产生者和响应者,以及因表达过高或过低而导致的疾病,对各种疾病的结果都有显著影响。在此,我们对 IL-22 进行了全面的回顾;从历史角度和最初的发现,以及最近的数据,这些数据极大地扩展了这种细胞因子的细胞来源和影响。我们的目的是展示 IL-22 的双重性,并强调 IL-22 在粘膜和组织屏障部位的串扰和影响领域存在的空白。
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引用次数: 0
Glioblastoma-associated macrophages: A key target in overcoming glioblastoma therapeutic resistance. 胶质母细胞瘤相关巨噬细胞:克服胶质母细胞瘤耐药性的关键靶点
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-31 DOI: 10.1016/j.cytogfr.2024.10.009
Aymane Kricha, Najat Bouchmaa, Sanae Ben Mkaddem, Abdellatif Abbaoui, Reda Ben Mrid, Rachid El Fatimy

Glioblastoma multiforme (GBM) is recognized as the most aggressive and malignant form of brain cancer, characterized by a highly heterogeneous phenotype, poor prognosis, and a median survival time of less than 16 months. Recent studies have highlighted the critical role of glioblastoma-associated macrophages (GAMs) in promoting tumor progression and resistance not only to immunotherapy but also to radiotherapy and chemotherapy. GAMs actively suppress immune responses, promote angiogenesis, facilitate tumor metastasis, and induce therapy resistance, through various mechanisms such as cytokines production, signaling pathways regulation, and angiogenesis. In this context, understanding these regulatory mechanisms is essential for developing efficient therapies. Preclinical studies have investigated diverse approaches to target these cells, both as monotherapies or in combination with other treatments. While these approaches have shown promise in strengthening antitumor immune responses in animal models, their clinical success remains to be fully determined. Herein, we provide a comprehensive overview of GAMs's role in GBM therapeutic resistance and summarizes existing approaches to target GAMs in overcoming tumor resistance.

多形性胶质母细胞瘤(GBM)被认为是最具侵袭性的恶性脑癌,其特点是表型高度异质性、预后差、中位生存期不到 16 个月。最近的研究突显了胶质母细胞瘤相关巨噬细胞(GAMs)在促进肿瘤进展和抵抗免疫疗法以及放疗和化疗方面的关键作用。GAMs 通过产生细胞因子、调节信号通路和血管生成等多种机制,积极抑制免疫反应、促进血管生成、促进肿瘤转移和诱导耐药性。在这种情况下,了解这些调控机制对于开发高效疗法至关重要。临床前研究已经研究了针对这些细胞的多种方法,既可作为单一疗法,也可与其他疗法联合使用。虽然这些方法已在动物模型中显示出加强抗肿瘤免疫反应的前景,但其临床成功与否仍有待全面确定。在此,我们全面概述了 GAMs 在 GBM 治疗耐药性中的作用,并总结了针对 GAMs 克服肿瘤耐药性的现有方法。
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引用次数: 0
The role of transforming growth factor β in cervical carcinogenesis. 转化生长因子β在宫颈癌变中的作用。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-22 DOI: 10.1016/j.cytogfr.2024.10.006
Kleber Paiva Trugilo, Guilherme Cesar Martelossi Cebinelli, Eliza Pizarro Castilha, Mariane Ricciardi da Silva, Fernanda Costa Brandão Berti, Karen Brajão de Oliveira

Human papillomavirus (HPV) is involved in virtually all cases of cervical cancer. However, HPV alone is not sufficient to cause malignant development. The effects of chronic inflammation and the interaction of immune components with the microenvironment infected with the high-risk HPV type (HR) may contribute to cancer development. Transforming growth factor β (TGFB) appears to play an important role in cervical carcinogenesis. Protein and mRNA levels of this cytokine gradually increase as normal tissue develops into malignant tissue and are closely related to the severity of HPV infection. At the onset of infection, TGFB can inhibit the proliferation of infected cells and viral amplification by inhibiting cell growth and downregulating the transcriptional activity of the long control region (LCR) of HPV, thereby reducing the expression of early genes. When infected cells progress to a malignant phenotype, the response to the cell growth inhibitory effect of TGFB1 is lost and the suppression of E6 and E7 expression decreases. Subsequently, TGFB1 expression is upregulated by high levels of E6 and E7 oncoproteins, leading to an increase in TGFB1 in the tumor microenvironment, where this molecule promotes epithelial-to-mesenchymal transition (EMT), cell motility, angiogenesis, and immunosuppression. This interaction between HPV oncoproteins and TGFB1 is an important mechanism promoting the development and progression of cervical cancer.

几乎所有宫颈癌病例都与人类乳头瘤病毒(HPV)有关。然而,仅靠 HPV 并不足以导致恶性发展。慢性炎症的影响以及免疫成分与感染高危型 HPV(HR)的微环境的相互作用可能会导致癌症的发生。转化生长因子β(TGFB)似乎在宫颈癌的发生中起着重要作用。当正常组织发展为恶性组织时,这种细胞因子的蛋白和 mRNA 水平会逐渐升高,并且与 HPV 感染的严重程度密切相关。在感染初期,TGFB 可通过抑制细胞生长和下调 HPV 长控制区(LCR)的转录活性,从而降低早期基因的表达,抑制感染细胞的增殖和病毒的扩增。当受感染的细胞发展到恶性表型时,TGFB1 对细胞生长抑制作用的反应就会消失,对 E6 和 E7 表达的抑制作用也会减弱。随后,高水平的 E6 和 E7 肿瘤蛋白会上调 TGFB1 的表达,导致肿瘤微环境中的 TGFB1 增加,而这种分子会促进上皮细胞向间质转化(EMT)、细胞运动、血管生成和免疫抑制。HPV 癌蛋白与 TGFB1 之间的这种相互作用是促进宫颈癌发生和发展的重要机制。
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引用次数: 0
Impact of chronic stress on intestinal mucosal immunity in colorectal cancer progression. 慢性压力对结直肠癌进展过程中肠粘膜免疫的影响
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-22 DOI: 10.1016/j.cytogfr.2024.10.007
Shengya Yang, Ying Li, Yingru Zhang, Yan Wang

Chronic stress is a significant risk factor that contributes to the progression of colorectal cancer (CRC) and has garnered considerable attention in recent research. It influences the distribution and function of immune cells within the intestinal mucosa through the "brain-gut" axis, altering cytokine and chemokine secretion and creating an immunosuppressive tumor microenvironment. The intestine, often called the "second brain," is particularly susceptible to the effects of chronic stress. Cytokines and chemokines in intestinal mucosal immunity(IMI) are closely linked to CRC cells' proliferation, metastasis, and drug resistance under chronic stress. Recently, antidepressants have emerged as potential therapeutic agents for CRC, possibly by modulating IMI to restore homeostasis and exert anti-tumor effects. This article reviews the role of chronic stress in promoting CRC progression via its impact on intestinal mucosal immunity, explores potential targets within the intestinal mucosa under chronic stress, and proposes new approaches for CRC treatment.

慢性压力是导致结直肠癌(CRC)恶化的一个重要风险因素,在最近的研究中引起了广泛关注。它通过 "脑-肠 "轴影响肠粘膜内免疫细胞的分布和功能,改变细胞因子和趋化因子的分泌,并形成免疫抑制性肿瘤微环境。肠道常被称为 "第二大脑",特别容易受到慢性压力的影响。肠粘膜免疫中的细胞因子和趋化因子(IMI)在慢性压力下,细胞因子和趋化因子与 CRC 细胞的增殖、转移和耐药性密切相关。最近,抗抑郁药成为治疗 CRC 的潜在药物,可能是通过调节 IMI 来恢复体内平衡并发挥抗肿瘤作用。本文回顾了慢性应激通过影响肠粘膜免疫促进 CRC 进展的作用,探讨了慢性应激下肠粘膜的潜在靶点,并提出了治疗 CRC 的新方法。
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引用次数: 0
Central role of Galectin-3 at the cross-roads of cardiac inflammation and fibrosis: Implications for heart failure and transplantation. Galectin-3 在心脏炎症和纤维化交叉点上的核心作用:对心力衰竭和移植的影响。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-20 DOI: 10.1016/j.cytogfr.2024.10.002
Ignacio M Seropian, Mohammad El-Diasty, Adham H El-Sherbini, Germán E González, Gabriel A Rabinovich

Cardiac inflammation and fibrosis are central pathogenic mechanisms leading to heart failure. Transplantation is still the treatment of choice for many patients undergoing end-stage heart failure who remain symptomatic despite optimal medical therapy. In spite of considerable progress, the molecular mechanisms linking inflammation, fibrosis and heart failure remain poorly understood. Galectin-3 (GAL3), a chimera-type member of the galectin family, has emerged as a critical mediator implicated in cardiac inflammatory, vascular and fibrotic processes through modulation of different cellular compartments including monocytes and macrophages, fibroblasts, endothelial cells and vascular smooth muscle cells via glycan-dependent or independent mechanisms. GAL3-driven circuits may hierarchically amplify cytokine production and function, immune cell activation and fibrosis cascades, influencing a wide range of cardiovascular disorders. Thus, GAL3 emerges as a potential therapeutic target to counteract aberrant inflammation and fibrosis during heart failure and a potential biomarker of heart failure and clinical outcome of heart transplantation.

心脏炎症和纤维化是导致心力衰竭的核心致病机制。对于许多接受最佳药物治疗后仍无症状的终末期心力衰竭患者来说,移植仍是首选治疗方法。尽管取得了相当大的进展,但人们对炎症、纤维化和心力衰竭之间的分子机制仍然知之甚少。Galectin-3(GAL3)是galectin家族的嵌合型成员,通过糖依赖或独立机制调节不同的细胞区,包括单核细胞和巨噬细胞、成纤维细胞、内皮细胞和血管平滑肌细胞,已成为与心脏炎症、血管和纤维化过程有关的关键介质。GAL3 驱动的回路可分层放大细胞因子的产生和功能、免疫细胞活化和纤维化级联,从而影响一系列心血管疾病。因此,GAL3 成为对抗心力衰竭期间异常炎症和纤维化的潜在治疗靶点,也是心力衰竭和心脏移植临床结果的潜在生物标志物。
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引用次数: 0
Unraveling the intricacies of neutrophil extracellular traps in inflammatory bowel disease: Pathways, biomarkers, and promising therapies. 揭开炎症性肠病中中性粒细胞胞外捕获物的神秘面纱:途径、生物标志物和有前景的疗法。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-18 DOI: 10.1016/j.cytogfr.2024.10.003
Yilin Wu, Jun Shen

The development of inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, involves various factors and is characterized by persistent inflammation of the mucosal lining. However, the role of neutrophils in this process remains controversial. Neutrophil extracellular traps (NETs), which consist of chromatin, antimicrobial proteins, and oxidative enzymes, are released by neutrophils to trap pathogens. They are also involved in various immune-mediated and vascular diseases. NETs act as a vital defense mechanisms at the gut-mucosal interface and are frequently exposed to bacterial, viral, and fungal threats. However, they can also contribute to inflammation and worsen imbalances in the gut bacteria. Recent studies have suggested that NETs have a significant impact on IBD development. Previous studies have shown increased levels of NETs in tissue and blood samples from patients with IBD, as well as in experimental colitis mouse models. Therefore, this review discusses how NETs are formed and their role in the pathophysiology of IBD. It discusses how NETs may lead to tissue damage and contribute to IBD-associated complications. Moreover, non-invasive biomarkers are needed to replace invasive procedures such as endoscopy to better evaluate the disease status. Given the crucial role of NETs in IBD progression, this review focuses on potential NET biomarkers that can help predict the evolution of IBD. Furthermore, this review identifies potential therapeutic targets for regulating NET production, which could expand the range of available treatment options for IBD.

包括溃疡性结肠炎和克罗恩病在内的炎症性肠病(IBD)的发病涉及多种因素,其特点是粘膜持续发炎。然而,中性粒细胞在这一过程中的作用仍存在争议。中性粒细胞释放的细胞外捕获物(NET)由染色质、抗菌蛋白和氧化酶组成,可捕获病原体。它们还与各种免疫介导的疾病和血管疾病有关。NET 是肠道粘膜界面的重要防御机制,经常受到细菌、病毒和真菌的威胁。然而,它们也会导致炎症,加剧肠道细菌的失衡。最近的研究表明,NET 对 IBD 的发展有重大影响。以往的研究表明,在 IBD 患者的组织和血液样本中,以及在实验性结肠炎小鼠模型中,NETs 的含量都有所增加。因此,本综述将讨论 NET 是如何形成的,以及它们在 IBD 病理生理学中的作用。它还讨论了 NET 如何导致组织损伤并引发 IBD 相关并发症。此外,还需要非侵入性生物标志物来取代内窥镜等侵入性检查,以更好地评估疾病状况。鉴于 NET 在 IBD 病程进展中的关键作用,本综述将重点关注有助于预测 IBD 演变的潜在 NET 生物标志物。此外,本综述还确定了调节 NET 生成的潜在治疗靶点,这将扩大 IBD 的可用治疗方案范围。
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引用次数: 0
Distinct roles of MIF in the pathogenesis of ischemic heart disease. MIF 在缺血性心脏病发病机制中的不同作用。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-16 DOI: 10.1016/j.cytogfr.2024.10.005
Ling Zhao, Bang-Hao Zhao, Amanguli Ruze, Qiu-Lin Li, An-Xia Deng, Xiao-Ming Gao

The role of macrophage migration inhibitory factor (MIF) as a multifunctional cytokine in immunomodulation and inflammatory response is increasingly appreciated. Ischemic heart disease (IHD), the leading cause of global mortality, remains a focal point of research owing to its intricate pathophysiology. MIF has been identified as a critical player in IHD, where it exerts distinct roles. On one hand, MIF plays a protective role by enhancing energy metabolism through activation of AMPK, resisting oxidative stress, inhibiting activation of the JNK pathway, and maintaining intracellular calcium ion homeostasis. Additionally, MIF exerts protective effects through mesenchymal stem cells and exosomes. On the other hand, MIF can assume a pro-inflammatory role, which contributes to the exacerbation of IHD's development and progression. Furthermore, MIF levels significantly increase in IHD patients, and its genetic polymorphisms are positively correlated with prevalence and severity. These findings position MIF as a potential biomarker and therapeutic target in the management of IHD. This review summarizes the structure, source, signaling pathways and biological functions of MIF and focuses on its roles and clinical characteristics in IHD. The genetic variants of MIF associated with IHD is also discussed, providing more understandings of its complex interplay in the disease's pathology.

巨噬细胞迁移抑制因子(MIF)是一种多功能细胞因子,在免疫调节和炎症反应中的作用日益受到重视。缺血性心脏病(IHD)是导致全球死亡的主要原因,由于其病理生理学错综复杂,它仍然是研究的焦点。MIF 被认为是缺血性心脏病的关键因素,在其中发挥着不同的作用。一方面,MIF 通过激活 AMPK 加强能量代谢、抵抗氧化应激、抑制 JNK 通路的激活以及维持细胞内钙离子的平衡,从而发挥保护作用。此外,MIF 还通过间充质干细胞和外泌体发挥保护作用。另一方面,MIF 可发挥促炎作用,从而加剧 IHD 的发展和恶化。此外,IHD 患者体内的 MIF 水平明显升高,其基因多态性与发病率和严重程度呈正相关。这些发现使 MIF 成为治疗 IHD 的潜在生物标志物和治疗靶点。本综述总结了 MIF 的结构、来源、信号传导途径和生物功能,并重点讨论了其在 IHD 中的作用和临床特征。此外,还讨论了与 IHD 相关的 MIF 基因变异,使人们对其在疾病病理中的复杂相互作用有了更多的了解。
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引用次数: 0
NLRP1 inflammasome in neurodegenerative disorders: From pathology to therapies. 神经退行性疾病中的 NLRP1 炎症小体:从病理学到疗法
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-16 DOI: 10.1016/j.cytogfr.2024.10.004
Meng-Jie Zhang, Long Yang, Zhuo-Yao Li, Long-Yun Zhou, Yong-Jun Wang, Hong-Shen Wang, Xue-Jun Cui, Min Yao

Neuroinflammation is a critical component in neurodegenerative disorders. The inflammasome, facilitates the cleavage of caspase-1, leading to the maturation and subsequent secretion of inflammatory factors interleukin (IL)-1β and IL-18. Consequently, pyroptosis mediated by gasdermin D, exacerbates neuroinflammation. Among the inflammasomes, NLRP1/3 are predominant in the central nervous system (CNS), Although NLRP1 was the earliest discovered inflammasome, the specific involvement of NLRP1 in neurodegenerative diseases remains to be fully elucidated. Recently, the discovery of an endogenous inhibitor of NLRP1, dipeptidyl peptidase 9, suggests the feasibility of producing of small-molecule drugs targeting NLRP1. This review describes the latest findings on the role of the NLRP1 inflammasome in the pathology of neurodegenerative disorders, including Alzheimer's disease, and summarises the regulatory mechanisms of NLRP1 inflammasome activation in the CNS. Furthermore, we highlight the recent progress in developing small-molecule and biological inhibitors that modulate the NLRP1 infammasome for the treatment of neurodegenerative disorders, some of which are advancing to preclinical testing. SIGNIFICANCE STATEMENT: The objective of this review is to synthesise the research on the structure, activation, and regulatory mechanisms of the NLRP1 inflammasome, along with its potential impact on both acute and chronic neurodegenerative conditions. The discovery of endogenous inhibitors, such as dipeptidyl peptidase 9 and thioredoxin, and their interaction with NLRP1 suggest the possibility of developing NLRP1-targeted small-molecule drugs for the treatment of neurodegenerative disorders. This review also discusses the use of both direct and indirect NLRP1 inhibitors as prospective therapeutic strategies for these conditions.

神经炎症是神经退行性疾病的重要组成部分。炎性体促进了 caspase-1 的裂解,导致炎性因子白细胞介素(IL)-1β 和 IL-18 的成熟和随后分泌。因此,由 gasdermin D 介导的脓毒症会加剧神经炎症。虽然 NLRP1 是最早被发现的炎性体,但 NLRP1 在神经退行性疾病中的具体参与仍有待全面阐明。最近,NLRP1 的内源性抑制剂--二肽基肽酶 9 的发现表明,生产针对 NLRP1 的小分子药物是可行的。本综述介绍了有关 NLRP1 炎症小体在神经退行性疾病(包括阿尔茨海默病)病理学中作用的最新发现,并总结了 NLRP1 炎症小体在中枢神经系统中激活的调控机制。此外,我们还重点介绍了最近在开发调节 NLRP1 炎症小体的小分子和生物抑制剂以治疗神经退行性疾病方面取得的进展,其中一些抑制剂已进入临床前测试阶段。意义声明:本综述旨在总结有关 NLRP1 炎症小体的结构、激活和调控机制的研究及其对急性和慢性神经退行性疾病的潜在影响。二肽基肽酶 9 和硫氧还蛋白等内源性抑制剂的发现及其与 NLRP1 的相互作用,为开发 NLRP1 靶向小分子药物治疗神经退行性疾病提供了可能。本综述还讨论了使用直接和间接 NLRP1 抑制剂作为这些疾病的前瞻性治疗策略。
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引用次数: 0
The Yin and Yang of TLR4 in COVID-19. TLR4 在 COVID-19 中的阴与阳。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-09 DOI: 10.1016/j.cytogfr.2024.10.001
Suprabhat Mukherjee, Jagadeesh Bayry

Various pattern recognition receptors (PRRs), including toll-like receptors (TLRs), play a crucial role in recognizing invading pathogens as well as damage-associated molecular patterns (DAMPs) released in response to infection. The resulting signaling cascades initiate appropriate immune responses to eliminate these pathogens. Current evidence suggests that SARS-CoV-2-driven activation of TLR4, whether through direct recognition of the spike glycoprotein (alone or in combination with endotoxin) or by sensing various TLR4-activating DAMPs or alarmins released during viral infection, acts as a critical mediator of antiviral immunity. However, TLR4 exerts a dual role in COVID-19, demonstrating both beneficial and deleterious effects. Dysregulated TLR4 signaling is implicated in the proinflammatory consequences linked to the immunopathogenesis of COVID-19. Additionally, TLR4 polymorphisms contribute to severity of the disease. Given its significant immunoregulatory impact on COVID-19 immunopathology and host immunity, TLR4 has emerged as a key target for developing inhibitors and immunotherapeutic strategies to mitigate the adverse effects associated with SARS-CoV-2 and related infections. Furthermore, TLR4 agonists are also being explored as adjuvants to enhance immune responses to SARS-CoV-2 vaccines.

包括收费样受体(TLRs)在内的各种模式识别受体(PRRs)在识别入侵病原体以及感染时释放的损伤相关分子模式(DAMPs)方面发挥着至关重要的作用。由此产生的信号级联启动适当的免疫反应,以消灭这些病原体。目前的证据表明,SARS-CoV-2 驱动的 TLR4 激活,无论是通过直接识别尖峰糖蛋白(单独或与内毒素结合),还是通过感知病毒感染过程中释放的各种 TLR4 激活 DAMP 或警报素,都是抗病毒免疫的关键介质。然而,TLR4 在 COVID-19 中发挥着双重作用,既有有益的影响,也有有害的影响。TLR4 信号传导失调与 COVID-19 免疫发病机制相关的促炎后果有关。此外,TLR4 多态性也会导致疾病的严重程度。鉴于 TLR4 对 COVID-19 免疫病理和宿主免疫具有重要的免疫调节作用,它已成为开发抑制剂和免疫治疗策略的关键靶点,以减轻与 SARS-CoV-2 和相关感染有关的不良影响。此外,TLR4 激动剂还被探索用作佐剂,以增强对 SARS-CoV-2 疫苗的免疫反应。
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引用次数: 0
Molecular mechanisms of regulation of IL-1 and its receptors. 调节 IL-1 及其受体的分子机制。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-05 DOI: 10.1016/j.cytogfr.2024.09.004
J V Zhukova, J A Lopatnikova, A A Alshevskaya, S V Sennikov

Interleukin 1 (IL-1) is a pro-inflammatory cytokine that plays a key role in the development and regulation of nonspecific defense and specific immunity. However, its regulatory influence extends beyond inflammation and impacts a range of immune and non-immune processes. The involvement of IL-1 in numerous biological processes, including modulation of inflammation, necessitates strict regulation at multiple levels. This review focuses on these regulatory processes and discusses their underlying mechanisms. IL-1 activity is controlled at various levels, including receptor binding, gene transcription, expression as inactive proforms, and regulated post-translational processing and secretion. Regulation at the level of the receptor expression - alternative splicing, tissue-specific isoforms, and gene polymorphism - is also crucial to IL-1 functional activity. Understanding these regulatory features of IL-1 will not only continue to shape future research directions but will also highlight promising therapeutic strategies to modulate the biological effects of IL-1.

白细胞介素 1(IL-1)是一种促炎细胞因子,在非特异性防御和特异性免疫的发展和调节中发挥着关键作用。然而,它的调节作用超出了炎症范围,对一系列免疫和非免疫过程都有影响。IL-1 参与了许多生物过程,包括炎症的调节,因此有必要在多个层面进行严格的调控。本综述将重点讨论这些调控过程及其内在机制。IL-1 的活性在不同水平上受到控制,包括受体结合、基因转录、以非活性原形表达以及翻译后处理和分泌调节。受体表达水平的调控--替代剪接、组织特异性异构体和基因多态性--对 IL-1 的功能活性也至关重要。了解 IL-1 的这些调控特征不仅将继续塑造未来的研究方向,还将凸显调节 IL-1 生物效应的有前途的治疗策略。
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引用次数: 0
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