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Understanding innate and adaptive responses during radiation combined burn injuries. 了解辐射合并烧伤时的先天反应和适应性反应。
IF 5 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-09-11 DOI: 10.1080/08830185.2024.2402023
Rishav Kumar,Ajay Kumar Sharma,Kirti,Aman Kalonia,Priyanka Shaw,M H Yashvarddhan,Arpana Vibhuti,Sandeep Kumar Shukla
The occurrence of incidents involving radiation-combined burn injuries (RCBI) poses a significant risk to public health. Understanding the immunological and physiological responses associated with such injuries is crucial for developing care triage to counter the mortality that occurs due to the synergistic effects of radiation and burn injuries. The core focus of this narrative review lies in unraveling the immune response against RCBI. Langerhans cells, mast cells, keratinocytes, and fibroblasts, which induce innate immunity, have been explored for their response to radiation, burns, and combined injuries. In the case of adaptive immune response, exploring behavioral changes in T regulatory (Treg) cells, T helper cells (Th1, Th2, and Th17), and immunoglobulin results in delayed healing compared to burn and radiation injury. The review also includes the function of complement system components such as neutrophils, acute phase proteins (CRP, C3, and C5), and cytokines for their role in RCBI. Combined insults resulting in a reduction in the cell population of immune cells display variation in response based on radiation doses, burn injury types, and their intrinsic radiosensitivity. The lack of approved countermeasures against RCBI poses a significant challenge. Drug repurposing might help to balance immune cell alteration, resulting in fast recovery and decreasing mortality, which gives it clinical significance for its implication on the site of such incidence. However, the exact immune response in RCBI remains insufficiently explored in pre-clinical and clinical stages, which might be due to the non-availability of in vitro models, standard animal models, or human subjects, warranting further research.
辐射复合烧伤(RCBI)事件的发生对公众健康构成了重大风险。了解与此类损伤相关的免疫和生理反应,对于制定护理分流方案以应对因辐射和烧伤的协同效应而造成的死亡至关重要。本综述的核心重点在于揭示针对 RCBI 的免疫反应。朗格汉斯细胞、肥大细胞、角质形成细胞和成纤维细胞可诱导先天性免疫,我们已对它们对辐射、烧伤和综合损伤的反应进行了研究。在适应性免疫反应方面,探讨了 T 调节(Treg)细胞、T 辅助细胞(Th1、Th2 和 Th17)和免疫球蛋白的行为变化,结果发现与烧伤和辐射损伤相比,愈合延迟。综述还包括补体系统成分的功能,如中性粒细胞、急性期蛋白(CRP、C3 和 C5)以及细胞因子在 RCBI 中的作用。由于辐射剂量、烧伤类型及其固有的辐射敏感性不同,导致免疫细胞数量减少的综合损伤会产生不同的反应。缺乏已获批准的 RCBI 对策是一项重大挑战。药物再利用可能有助于平衡免疫细胞的改变,从而快速康复并降低死亡率,这对此类疾病的发病部位具有重要的临床意义。然而,在临床前和临床阶段,RCBI 的确切免疫反应仍未得到充分探索,这可能是由于没有体外模型、标准动物模型或人体受试者,因此需要进一步研究。
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引用次数: 0
Immunological processes of enhancers and suppressors of long non-coding RNAs associated with brain tumors and inflammation. 与脑肿瘤和炎症相关的长链非编码rna的增强子和抑制子的免疫过程。
IF 5 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-05-01 Epub Date: 2023-11-17 DOI: 10.1080/08830185.2023.2280581
Hossein Tahmasebi Dehkordi, Fatemeh Khaledi, Sorayya Ghasemi

Immunological processes, such as inflammation, can both cause tumor suppression and cancer progression. Moreover, deregulated levels of long non-coding RNA (lncRNA) expression in the brain may cause inflammation and lead to the growth of tumors. Like other biological processes, the immune system's role in cancer is complicated, varies, and can help or hurt the cancer's maintenance. According to research, inflammation and brain cancer are correlated via several signaling pathways. A variety of lncRNAs have recently been revealed to influence cancer by modulating inflammatory pathways. As a result, lncRNAs have the potential to influence carcinogenesis, tumor formation, or tumor suppression via an increase or decrease in inflammation functions. Although the study and targeting of lncRNAs have made great progress in the treatment of cancer, there are definitely limitations and challenges. Using new technologies like nanocarriers and cell-penetrating peptides (CPPs) to target treatments without hurting healthy body tissues has shown to be very effective. In this review article, we have collected significantly related lncRNAs and their inhibitory or stimulating roles in inflammation and brain cancer for the first time. However, there are limitations, such as side effects and damage to normal tissues. With the advancement of new targeting technologies, these lncRNAs may be candidates for the specific targeting therapy of brain cancers by limiting inflammation or stimulating the immune system against them in the future.

免疫过程,如炎症,既可以抑制肿瘤又可以导致癌症进展。此外,大脑中长链非编码RNA (lncRNA)表达水平的失调可能引起炎症并导致肿瘤的生长。像其他生物过程一样,免疫系统在癌症中的作用是复杂的,多变的,可以帮助或损害癌症的维持。根据研究,炎症和脑癌通过几种信号通路相互关联。最近发现多种lncrna通过调节炎症途径影响癌症。因此,lncRNAs有可能通过增加或减少炎症功能来影响致癌、肿瘤形成或肿瘤抑制。尽管lncrna的研究和靶向治疗在癌症治疗方面取得了很大进展,但也存在一定的局限性和挑战。使用纳米载体和细胞穿透肽(CPPs)等新技术来靶向治疗而不伤害健康的身体组织已被证明是非常有效的。在这篇综述文章中,我们首次收集到显著相关的lncrna及其在炎症和脑癌中的抑制或刺激作用。然而,也有局限性,比如副作用和对正常组织的损伤。随着新的靶向技术的进步,这些lncrna可能成为未来脑癌特异性靶向治疗的候选者,通过限制炎症或刺激免疫系统来对抗它们。
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引用次数: 0
Low-dose IL-2 therapy in autoimmune diseases: An update review. 低剂量IL-2治疗自身免疫性疾病:最新综述。
IF 5 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-05-01 Epub Date: 2023-10-26 DOI: 10.1080/08830185.2023.2274574
Ruizhi Zhang, Yuyang Zhao, Xiangming Chen, Zhuoqing Zhuang, Xiaomin Li, Erxia Shen

Regulatory T (Treg) cells are essential for maintaining self-immune tolerance. Reduced numbers or functions of Treg cells have been involved in the pathogenesis of various autoimmune diseases and allograft rejection. Therefore, the approaches that increase the pool or suppressive function of Treg cells in vivo could be a general strategy to treat different autoimmune diseases and allograft rejection. Interleukin-2 (IL-2) is essential for the development, survival, maintenance, and function of Treg cells, constitutively expressing the high-affinity receptor of IL-2 and sensitive response to IL-2 in vivo. And low-dose IL-2 therapy in vivo could restore the imbalance between autoimmune response and self-tolerance toward self-tolerance via promoting Treg cell expansion and inhibiting follicular helper T (Tfh) and IL-17-producing helper T (Th17) cell differentiation. Currently, low-dose IL-2 treatment is receiving extensive attention in autoimmune disease and transplantation treatment. In this review, we summarize the biology of IL-2/IL-2 receptor, the mechanisms of low-dose IL-2 therapy in autoimmune diseases, the application in the progress of different autoimmune diseases, including Systemic Lupus Erythematosus (SLE), Type 1 Diabetes (T1D), Rheumatoid Arthritis (RA), Autoimmune Hepatitis (AIH), Alopecia Areata (AA), Immune Thrombocytopenia (ITP) and Chronic graft-versus-host-disease (GVHD). We also discuss the future directions to optimize low-dose IL-2 treatments.

调节性T细胞(Treg)对维持自身免疫耐受至关重要。Treg细胞数量或功能的减少参与了各种自身免疫性疾病和同种异体移植物排斥反应的发病机制。因此,增加体内Treg细胞库或抑制功能的方法可能是治疗不同自身免疫性疾病和同种异体移植物排斥反应的通用策略。白细胞介素-2(IL-2)对Treg细胞的发育、生存、维持和功能至关重要,在体内组成性表达IL-2的高亲和力受体和对IL-2的敏感反应。体内低剂量IL-2治疗可以通过促进Treg细胞扩增和抑制卵泡辅助T(Tfh)和产生IL-17的辅助T(Th17)细胞分化来恢复自身免疫反应和自我耐受之间对自我耐受的失衡。目前,低剂量IL-2治疗在自身免疫性疾病和移植治疗中受到广泛关注。在这篇综述中,我们总结了IL-2/IL-2受体的生物学、低剂量IL-2治疗自身免疫性疾病的机制,以及在不同自身免疫疾病进展中的应用,包括系统性红斑狼疮(SLE)、1型糖尿病(T1D)、类风湿性关节炎(RA)、自身免疫性肝炎(AIH)、斑秃(AA),免疫性血小板减少症(ITP)和慢性移植物抗宿主病(GVHD)。我们还讨论了优化低剂量IL-2治疗的未来方向。
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引用次数: 0
STATs signaling pathways in dendritic cells: As potential therapeutic targets? 树突状细胞中的STATs信号通路:作为潜在的治疗靶点?
IF 5 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-05-01 Epub Date: 2023-10-27 DOI: 10.1080/08830185.2023.2274576
Sepideh Sohrabi, Javad Masoumi, Bahar Naseri, Farid Ghorbaninezhad, Shiva Alipour, Tohid Kazemi, Javad Ahmadian Heris, Leili Aghebati Maleki, Pedram Basirjafar, Raziyeh Zandvakili, Mohammad Amin Doustvandi, Behzad Baradaran

Dendritic cells (DCs) are professional antigen-presenting cells (APCs), including heterogenous populations with phenotypic and functional diversity that coordinate bridging innate and adaptive immunity. Signal transducer and activator of transcriptions (STAT) factors as key proteins in cytokine signaling were shown to play distinct roles in the maturation and antigen presentation of DCs and play a pivotal role in modulating immune responses mediated by DCs such as differentiation of T cells to T helper (Th) 1, Th2 or regulatory T (Treg) cells. This review sheds light on the importance of STAT transcription factors' signaling pathways in different subtypes of DCs and highlights their targeting potential usages for improving DC-based immunotherapies for patients who suffer from cancer or diverse autoimmune conditions according to the type of the STAT transcription factor and its specific activating or inhibitory agent.

树突状细胞(DC)是专业的抗原呈递细胞(APC),包括具有表型和功能多样性的异质群体,协调先天免疫和适应性免疫。信号转导子和转录激活子(STAT)因子作为细胞因子信号传导中的关键蛋白,在DC的成熟和抗原呈递中发挥着不同的作用,并在调节DC介导的免疫反应中发挥着关键作用,如T细胞分化为T辅助细胞(Th)1、Th2或调节性T细胞(Treg)。这篇综述阐明了STAT转录因子信号通路在不同亚型DC中的重要性,并强调了其靶向潜在用途,根据STAT转录因素的类型及其特异性激活或抑制剂,改善癌症或多种自身免疫疾病患者的DC基免疫疗法。
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引用次数: 0
RNA methylation: A potential therapeutic target in autoimmune disease. RNA甲基化:自身免疫性疾病的潜在治疗靶点
IF 4.3 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-05-01 Epub Date: 2023-11-17 DOI: 10.1080/08830185.2023.2280544
Lele Li, Xiaoping Xia, Tian Yang, Yuchao Sun, Xueke Liu, Wei Xu, Mei Lu, Dawei Cui, Yingping Wu

Autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and inflammatory bowel disease (IBD) are caused by the body's immune response to autoantigens. The pathogenesis of autoimmune diseases is unclear. Numerous studies have demonstrated that RNA methylation plays a key role in disease progression, which is essential for post-transcriptional regulation and has gradually become a broad regulatory mechanism that controls gene expression in various physiological processes, including RNA nuclear output, translation, splicing, and noncoding RNA processing. Here, we outline the writers, erasers, and readers of RNA methylation, including N6-methyladenosine (m6A), 2'-O-methylation (Nm), 2'-O-dimethyladenosine (m6Am), N1-methyladenosine (m1A), 5-methylcytidine (m5C) and N7-methylguanosine (m7G). As the role of RNA methylation modifications in the immune system and diseases is explained, the potential treatment value of these modifications has also been demonstrated. This review reports the relationship between RNA methylation and autoimmune diseases, highlighting the need for future research into the therapeutic potential of RNA modifications.

自身免疫性疾病如类风湿关节炎(RA)、系统性红斑狼疮(SLE)和炎症性肠病(IBD)是由机体对自身抗原的免疫反应引起的。自身免疫性疾病的发病机制尚不清楚。大量研究表明,RNA甲基化在疾病进展中起着关键作用,对转录后调控至关重要,并逐渐成为控制RNA核输出、翻译、剪接、非编码RNA加工等多种生理过程中基因表达的广泛调控机制。在这里,我们概述了RNA甲基化的书写器、擦除器和读取器,包括n6 -甲基腺苷(m6A)、2'- o -甲基化(Nm)、2'- o -二甲基腺苷(m6Am)、n1 -甲基腺苷(m1A)、5-甲基胞苷(m5C)和n7 -甲基鸟苷(m7G)。随着RNA甲基化修饰在免疫系统和疾病中的作用被解释,这些修饰的潜在治疗价值也被证明。这篇综述报道了RNA甲基化与自身免疫性疾病之间的关系,强调了未来研究RNA修饰治疗潜力的必要性。
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引用次数: 0
Cerebral malaria pathogenesis: Dissecting the role of CD4+ and CD8+ T-cells as major effectors in disease pathology 脑疟疾发病机制:剖析 CD4+ 和 CD8+ T 细胞作为主要效应因子在疾病病理学中的作用
IF 5 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-04-15 DOI: 10.1080/08830185.2024.2336539
Indu Sharma, Poonam Kataria, Jyoti Das
Cerebral malaria (CM) is a severe complication of Plasmodium falciparum (P. falciparum) infection, with complex pathogenesis involving multiple factors, including the host’s immunological response....
脑疟疾(CM)是恶性疟原虫(P. falciparum)感染的一种严重并发症,发病机制复杂,涉及多种因素,包括宿主的免疫反应....。
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引用次数: 0
The emerging role of T helper 9 (Th9) cells in immunopathophysiology: A comprehensive review of their effects and responsiveness in various disease states. T 辅助细胞 9 (Th9) 在免疫病理生理学中的新作用:全面回顾它们在各种疾病状态中的作用和反应。
IF 4.3 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-06-12 DOI: 10.1080/08830185.2024.2364586
Manoj Khokhar, Purvi Purohit

Th9 cells, a subset of T-helper cells producing interleukin-9 (IL-9), play a vital role in the adaptive immune response and have diverse effects in different diseases. Regulated by transcription factors like PU.1 and IRF4, and cytokines such as IL-4 and TGF-β, Th9 cells drive tissue inflammation. This review focuses on their emerging role in immunopathophysiology. Th9 cells exhibit immune-mediated cancer cell destruction, showing promise in glioma and cervical cancer treatment. However, their role in breast and lung cancer is intricate, requiring a deeper understanding of pro- and anti-tumor aspects. Th9 cells, along with IL-9, foster T cell and immune cell proliferation, contributing to autoimmune disorders. They are implicated in psoriasis, atopic dermatitis, and infections. In allergic reactions and asthma, Th9 cells fuel pro-inflammatory responses. Targeting Foxo1 may regulate innate and adaptive immune responses, alleviating disease symptoms. This comprehensive review outlines Th9 cells' evolving immunopathophysiological role, emphasizing the necessity for further research to grasp their effects and potential therapeutic applications across diseases.

Th9细胞是产生白细胞介素-9(IL-9)的T辅助细胞亚群,在适应性免疫反应中发挥着重要作用,并对不同疾病产生不同影响。在 PU.1 和 IRF4 等转录因子以及 IL-4 和 TGF-β 等细胞因子的调控下,Th9 细胞驱动组织炎症。本综述将重点讨论它们在免疫病理生理学中新出现的作用。Th9 细胞具有免疫介导的癌细胞破坏作用,在胶质瘤和宫颈癌治疗中大有可为。然而,Th9 细胞在乳腺癌和肺癌中的作用错综复杂,需要对其促癌和抗癌方面有更深入的了解。Th9细胞与IL-9一起促进T细胞和免疫细胞增殖,导致自身免疫性疾病。它们与牛皮癣、特应性皮炎和感染有关。在过敏反应和哮喘中,Th9 细胞会助长促炎反应。靶向 Foxo1 可调节先天性和适应性免疫反应,减轻疾病症状。这篇全面的综述概述了 Th9 细胞不断演变的免疫病理生理学作用,强调了进一步研究的必要性,以掌握它们在各种疾病中的作用和潜在治疗应用。
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引用次数: 0
STAT4 and STAT6, their role in cellular and humoral immunity and in diverse human diseases. STAT4 和 STAT6,它们在细胞和体液免疫以及各种人类疾病中的作用。
IF 4.3 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-08-26 DOI: 10.1080/08830185.2024.2395274
Manlio Tolomeo, Antonio Cascio

Signal transducer and activator of transcription (STAT) 4 and STAT6 play a crucial role in immune cells by transducing signals from specific cytokine receptors, and inducing transcription of genes involved in cell-mediated and humoral immunity. These two different defense mechanisms against pathogens are regulated by two specific CD4+ T helper (Th) cells known as Th1 and Th2 cells. Many studies have shown that several diseases including cancer, inflammatory, autoimmune and allergic diseases are associated with a Th1/Th2 imbalance caused by increased or decreased expression/activity of STAT4 or STAT6 often due to genetic and epigenetic aberrances. An altered expression of STAT4 has been observed in different tumors and autoimmune diseases, while a dysregulation of STAT6 signaling pathway is frequently observed in allergic conditions, such as atopic dermatitis, allergic asthma, food allergy, and tumors such as Hodgkin and non-Hodgkin lymphomas. Recently, dysregulations of STAT4 and STAT6 expression have been observed in SARS-CoV2 and monkeypox infections, which are still public health emergencies in many countries. SARS-CoV-2 can induce an imbalance in Th1 and Th2 responses with a predominant activation of STAT6 in the cytosol and nuclei of pneumocytes that drives Th2 polarization and cytokine storm. In monkeypox infection the virus can promote an immune evasion by inducing a Th2 response that in turn inhibits the Th1 response essential for virus elimination. Furthermore, genetic variations of STAT4 that are associated with an increased risk of developing systemic lupus erythematosus seem to play a role in defense against SARS-CoV-2 infection.

信号转导和激活转录(STAT)4 和 STAT6 在免疫细胞中发挥着至关重要的作用,它们从特定的细胞因子受体转导信号,并诱导参与细胞介导免疫和体液免疫的基因转录。这两种针对病原体的不同防御机制是由两种被称为 Th1 和 Th2 细胞的特定 CD4+ T 辅助(Th)细胞调控的。许多研究表明,包括癌症、炎症性疾病、自身免疫性疾病和过敏性疾病在内的多种疾病都与 Th1/Th2 失衡有关,而这种失衡是由 STAT4 或 STAT6 的表达/活性增高或降低(通常是由于遗传和表观遗传失常造成的)引起的。在不同的肿瘤和自身免疫性疾病中观察到 STAT4 表达的改变,而在过敏性疾病(如特应性皮炎、过敏性哮喘、食物过敏)和肿瘤(如霍奇金淋巴瘤和非霍奇金淋巴瘤)中经常观察到 STAT6 信号通路的失调。最近,在SARS-CoV2和猴痘感染中观察到STAT4和STAT6表达失调,这两种疾病在许多国家仍是突发公共卫生事件。SARS-CoV-2 可诱导 Th1 和 Th2 反应失衡,STAT6 在肺炎细胞的细胞膜和细胞核中被激活,从而推动 Th2 极化和细胞因子风暴。在猴痘感染中,病毒可通过诱导 Th2 反应促进免疫逃避,而 Th2 反应反过来又会抑制消除病毒所必需的 Th1 反应。此外,STAT4 基因变异会增加患系统性红斑狼疮的风险,这种变异似乎在抵御 SARS-CoV-2 感染方面发挥了作用。
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引用次数: 0
Orchestration of immune response by innate lymphoid cell subtype 2 at various tumor microenvironment, a suitable target for cancer immunotherapy. 先天性淋巴细胞亚型 2 在各种肿瘤微环境中协调免疫反应,是癌症免疫疗法的合适靶点。
IF 5 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2023-08-21 DOI: 10.1080/08830185.2023.2247021
Rajdeep Roy, Tanmoy Das, Nabendu Biswas

Innate lymphoid cells are a mixed population of cells and critical regulators of our innate immune system. According to recent scientific literature, tissue resident innate lymphoid cell subtype 2 has been recognized as an important player of type 2 inflammatory responses, involved in different human malignancies like pancreatic, lung, acute myeloid leukemia, gastrointestinal tract cancer, etc. The current reports have revealed that, among the three main ILC sub types, subtype 2 (ILC 2), as the key regulator of initiating the type 2 inflammatory responses at the tumor microenvironment (TME). This activation of ILC-2 is a very important step for the specific downstream functioning of ILC-2. Priming of ILC-2 with different chemokines involves different cytokine secretion from the activated ILC-2 like IL-4, IL-5, IL-13, IL-9 which induce type 2 inflammatory responses involved in the complex interaction with other immune cells like NK cell, Cytotoxic T cell, MDSC and Treg cell. At the initial stage, ILC-2 activation through IL-33 may induce the anti-tumorigenic effect mediated by ILC-2/eosinophil axis. However, it is also evident that PDG2 (Prostaglandin D2)-mediated activation of ILC-2 induces the ILC-2/MDSC immune suppressive pro-tumorigenic niche at the TME. Here, in this review, we have summarized the function of ILC-2 on cancer immunity based on recent scientific work which indicates ILC-2 plays a dual role and orchestrates the immune responses toward type 2 immunity in different cancer settings.

先天性淋巴细胞是一种混合细胞群,也是先天性免疫系统的关键调节因子。根据最近的科学文献,组织常驻先天性淋巴细胞亚型 2 被认为是第二类炎症反应的重要参与者,参与了胰腺癌、肺癌、急性髓性白血病、胃肠道癌等不同人类恶性肿瘤的治疗。目前的报告显示,在三种主要的 ILC 亚型中,亚型 2(ILC 2)是在肿瘤微环境(TME)中启动 2 型炎症反应的关键调节因子。激活 ILC-2 是 ILC-2 发挥特定下游功能的重要步骤。用不同的趋化因子激活 ILC-2,活化的 ILC-2 会分泌不同的细胞因子,如 IL-4、IL-5、IL-13、IL-9,从而诱发 2 型炎症反应,并与 NK 细胞、细胞毒性 T 细胞、MDSC 和 Treg 细胞等其他免疫细胞发生复杂的相互作用。在初期阶段,ILC-2 通过 IL-33 激活可能会诱导 ILC-2/ 嗜酸性粒细胞轴介导的抗肿瘤作用。然而,PDG2(前列腺素 D2)介导的 ILC-2 激活在 TME 诱导 ILC-2/MDSC 的免疫抑制促致癌龛也是显而易见的。在本综述中,我们根据最近的科学研究总结了ILC-2在癌症免疫中的功能,这些研究表明ILC-2在不同的癌症环境中扮演着双重角色,并协调着对2型免疫的免疫反应。
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引用次数: 0
Cholesterol: A friend to viruses. 胆固醇病毒的朋友
IF 5 4区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-02-19 DOI: 10.1080/08830185.2024.2314577
Yingchun Wang, Lifen Gao

Cholesterol is a key life-sustaining molecule which regulates membrane fluidity and serves as a signaling mediator. Cholesterol homeostasis is closely related to various pathological conditions including tumor, obesity, atherosclerosis, Alzheimer's disease and viral infection. Viral infection disrupts host cholesterol homeostasis, facilitating their own survival. Meanwhile, the host cells strive to reduce cholesterol accessibility to limit viral infection. This review focuses on the regulation of cholesterol metabolism and the role of cholesterol in viral infection, specifically providing an overview of cholesterol as a friend to promote viral entry, replication, assembly, release and immune evasion, which might inspire valuable thinking for pathogenesis and intervention of viral infection.

胆固醇是一种维持生命的关键分子,它能调节膜的流动性并充当信号介质。胆固醇平衡与各种病理状况密切相关,包括肿瘤、肥胖、动脉粥样硬化、阿尔茨海默病和病毒感染。病毒感染会破坏宿主细胞的胆固醇平衡,从而促进宿主细胞的生存。与此同时,宿主细胞努力降低胆固醇的可及性,以限制病毒感染。本综述侧重于胆固醇代谢的调控和胆固醇在病毒感染中的作用,特别是概述了胆固醇作为促进病毒进入、复制、组装、释放和免疫逃避的朋友,这可能会启发人们对病毒感染的发病机制和干预进行有价值的思考。
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引用次数: 0
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International Reviews of Immunology
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