IRAK—M在TLRs信号转导中负性调节作用的研究进展

白细胞介素1受体相关激酶（interleukin-1 receptor-associatd kinase,IRAK）家族被认为是TLR／IL-1R信号通路中重要的信号分子。迄今为止,已发现4个IRAK家族成员,其中IRAK-1和IRAK．4有激酶活性,IRAK-2和IRAK-M无激酶活性。最近的研究发现IRAK-M参与负性调控TLR信号通路和具有天然免疫的作用。本文就IRAK—M的结构特点及在TLR信号转导的分子机制和免疫耐受中的作用进行综述。     

益生菌抑制肠道慢性炎症及维持肠道稳态的研究进展

益生菌在维护健康和预防疾病方面起着重要作用。近30年来,人们对益生菌的特性、分类、分布与营养等方面的研究很多,特别是益生菌抑制肠道慢性炎症及维持肠道稳态方面的作用引起了国内外学者的广泛关注。近几年来,随着分子生物学技术的迅速发展,关于益生菌抑制肠道慢性炎症及维持肠道稳态方面的作用机制成为当前研究的热点,并取得了一定的成果。本文目的在于对益生菌抑制肠道慢性炎症及维持肠道稳态的作用进行分析。     

不同严重程度溃疡性结肠炎患者机体炎症状态和TLRs表达与肠道菌群失调的相关性

目的 探讨不同严重程度溃疡性结肠炎（UC）患者机体炎症状态和Toll样受体（TLRs）表达与肠道菌群紊乱的关系。方法 选取2021年1月至2022年1月我院诊治的102例UC患者作为研究组,以同期50例体格检查健康者作为对照组,对两组受试者的肠道菌群进行检测,同时检测患者TLR2、TLR4、TLR5、TLR9以及C反应蛋白（CRP）、白细胞介素（IL）6表达水平。指标间的关系采用Pearson相关性分析。结果 研究组患者肠道双歧杆菌、嗜酸乳杆菌、拟杆菌数量均低于对照组,大肠埃希菌、肠球菌数量均高于对照组,且研究组中活动期患者肠道双歧杆菌、嗜酸乳杆菌、拟杆菌数量低于缓解期患者,而大肠埃希菌、肠球菌数量均高于缓解期患者（均P<0.05）。研究组患者TLR2、TLR4、TLR5、TLR9相对表达量均高于对照组,且研究组中活动期患者TLRs相对表达量均高于缓解期患者（均P<0.05）。研究组患者CRP、IL-6水平均高于对照组,且研究组中活动期患者CRP、IL-6水平均高于缓解期患者（均P<0.05）。Pearson相关性分析结果显示,不同疾病严重程度UC患者机体炎症状态和T...     

肥胖与慢性炎症

肥胖及其相关的代谢类疾病严重影响人类的健康,而肥胖诱导的慢性炎症是胰岛素抵抗和代谢综合症发病的关键因素.脂肪组织慢性炎症发生的机制及其与代谢综合症的关系已经成为全球瞩目的研究热点.慢性炎症的特征主要包括脂肪组织中促炎细胞因子表达量增加,抗炎细胞因子表达量降低以及大量巨噬细胞浸润.鉴于肥胖及其相关代谢综合症对人类健康的巨大危害,现对慢性炎症的发生机制,肥胖和慢性炎症之间的关系,脂肪组织炎症中巨噬细胞浸润以及和信号传导通路进行综述.     

慢性炎症、自身免疫和动脉粥样硬化

动脉粥样硬化是一种炎症性疾病。在粥样斑块中存在许多免疫细胞,而且在不稳定斑块中尤为丰富。近年来对动脉粥样硬化中免疫细胞的聚集,分化和激活有了更深入的了解。流行病研究发现了多种与其相关的病毒和细菌感染。通过研究初步研究了几个自身性抗原,并提出了自身免疫假说。根据这些新的认识,提出了免疫调节和预防接种等心血管疾病的预防和治疗策略。这必将极大地提高对动脉粥样硬化的研究和防治水平。     

TIPE2在炎症、免疫相关疾病和肿瘤中的研究进展

肿瘤坏死因子-α诱导蛋白8样分子2(tumor necrosis factor-α-induced protein 8-like 2,TIPE2)是一种新型的先天免疫和细胞免疫的调节因子。TIPE2负向调节Toll样受体和T细胞受体的功能,其在免疫系统的选择性表达可抑制炎症反应并维持免疫稳态。大量研究表明,TIPE2是多种肿瘤生成和肿瘤免疫平衡动态调节的负性调节分子,是自然杀伤(natural killer,NK)细胞成熟和抗肿瘤免疫的潜在检查点。TIPE2在炎症、免疫相关疾病和肿瘤的发生发展过程中起重要作用,具有作为临床生物标志物的潜力。本文总结了TIPE2的结构特点、生物学功能及其在疾病中的异常表达和临床意义,为疾病治疗提供新的策略。     

炎症与肿瘤的关系研究进展

炎症与肿瘤关系密切,慢性炎症与1/4以上癌症发生相关.炎症微环境中细胞因子,自由基,前列腺素,生长因子等炎性应答介质能诱导DNA甲基化,抑癌基因点突变和翻译后修饰等基因和表观学变化,引起维持正常细胞内环境稳定关健通路的改变并导致癌症的发生和演进;近年来,对炎症中microRNA和免疫应答相互作用的研究进一步加深了人们对炎症与肿瘤相关性的了解.本文就炎症与肿瘤的间的桥梁分子予以综述,鉴定这些关键细胞成分及相互通路特异性的改变能为炎症相关性肿瘤的早期诊断、预防和治疗提供分子靶标.     

慢性炎症与甲状腺癌关系的研究进展

甲状腺癌是内分泌系统恶性肿瘤中最为常见的类型,其发病率约占90％,且仍有上升趋势。近年来,随着免疫学技术及分子生物学技术的快速发展和人类对甲状腺癌发病机制认识的不断深入,慢性炎症与甲状腺癌的相关性引起了大家的广泛关注。因此,本文就慢性炎症与甲状腺癌的最新研究进展进行综述。     

炎症细胞因子与慢性阻塞性肺疾病

慢性阻塞性肺疾病（chronic obstructive pulmonary dis-ease,COPD）不可否认是一个重要的世界卫生问题。对于它的发病机制目前尚未明了,普遍认同的观点有：（1）感染假说;（2）免疫失衡及炎症假说;（3）氧化损伤假说;（4）蛋白酶和抗蛋白酶失衡[1]。     

Toll-like receptors: A pathway alluding to cancer control

Toll-like receptors (TLRs) are usually expressed on immune cells such as macrophages, dendritic cells, mast cells, as well as on eosinophils and some epithelial cells. They play a central role in the recognition of harmful molecules that belong to invading microorganisms or internal damaged tissues, which lead to inflammation. Among the hallmarks of cancer, there is immune evasion and inflammation. Summing this with the discovery that a majority of cancers also seem to express TLRs, made researchers realize these receptors might also be linked with cancer progression. This review will cover some of the effects of TLR engagement in cancer cells that might induce the promotion or inhibition of cancer with mechanisms involved. The differences of TLR expression in cancer progression and its possible relation with patient prognosis, TLR genetic disorders found in cancer, and new strategies to cancer therapy will be discussed to target TLRs in cancer cells.     

Toll-like receptors and innate immunity

Toll-like receptors (TLRs) are evolutionarily conserved innate receptors expressed in various immune and non-immune cells of the mammalian host. TLRs play a crucial role in defending against pathogenic microbial infection through the induction of inflammatory cytokines and type I interferons. Furthermore, TLRs also play roles in shaping pathogen-specific humoral and cellular adaptive immune responses. In this review, we describe the recent advances in pathogen recognition by TLRs and TLR signaling.     

Viruses and Toll-like receptors

Production of inflammatory cytokines and type I interferons by mammalian cells is mediated through virus-specific activation of Toll-like receptors (TLRs). Known roles for different TLRs and speculation as to their roles in viral pathogenesis and immunity are discussed in this review.     

The role of Toll-like receptors in non-infectious lung injury

The role of Toll-like receptors （TLRs） in pathogen recognition has been expeditiously advanced in recent years. However, investigations into the function of TLRs in non-infectious tissue injury have just begun. Previously, we and others have demonstrated that fragmented hyaluronan （HA） accumulates during tissue injury. CD44 is required to clear HA during tissue injury, and impaired clearance of HA results in unremitting inflammation. Additionally, fragmented HA stimulates the expression of inflammatory genes by inflammatory cells at the injury site. Recently, we identified that HA fragments require both TLR2 and TLR4 to stimulate mouse macrophages to produce inflammatory chemokines and cytokines. In a non-infectious lung injury model, mice deficient in both TLR2 and TLR4 show an impaired transepithelial migration of inflammatory cells, increased tissue injury, elevated lung epithelial cell apoptosis, and decreased survival. Lung epithelial cell overexpression of high molecular mass HA protected mice against acute lung injury and apoptosis, in part through TLR-dependent basal activation of NF-κB. The exaggerated injury in TLR2 and TLR4 deficient mice appears to be due to impaired HA-TLR interactions on epithelial cells. These studies identify that host matrix component HA and TLR interactions provide signals that initiate inflammatory responses, maintain epithelial cell integrity, and promote recovery from acute lung injury.     

Toll-like receptors signaling in glomerular diseases

Abstract

Toll-like receptors (TLRs) are pattern-recognition receptors that recognize microbial/vial-derived components that trigger innate immune response, which indicate these molecules play a role in host defense against infection. The infection often precedes numerous disorders including glomerular diseases (glomerulonephritis (GN)). It is reported that TLRs are also involved in the risk and progression of GN, and TLRs may be potential therapeutic targets for GN. To date, a number of studies have found that TLRs are involved in the pathogenesis of GN. There is a paucity of reviews in the literature discussing signaling pathways and gene expression for TLRs in GN. This review was performed to provide a relatively complete signaling pathway flowchart for TLRs to the investigators who were interested in the roles of TLRs in the pathogenesis of GN. In the past decades, some studies were also performed to explore the association of TLRs gene expression with the risk of GN. However, the role of TLRs in the pathogenesis of GN remains controversial. Here, the signal transduction pathways of TLRs and its role of gene expression in the pathogenesis of GN were reviewed.     

Toll-like receptors (TLRs): An old family of immune receptors with a new face in cancer pathogenesis

In the dark path of tumorigenesis, the more carefully the cancer biology is studied, the more brilliant answers could be given to the countless questions about its orchestrating derivers. The identification of the correlation between Toll-like receptors (TLRs) and different processes involved in carcinogenesis was one of the single points of blinding light highlighting the interconnection between the immune system and cancer. TLRs are a wide family of single-pass membrane-spanning receptors that have developed through the evolution to recognize the structurally conserved molecules derived from microorganisms or damaged cells. But this is not everything about these receptors as they could orchestrate several downstream signalling pathways leading to the formation or suppression of cancer cells. The present review is tempted to provide a concise schematic about the biology and the characters of TLRs and also summarize the major findings of the regulatory role of TLRs and their associated signalling in the pathogenesis of human cancers.     

Role of toll-like receptors in lung cancer

Abstract

Lung cancer is a leading cause of death world-wide and the long-term survival rate for patients with lung cancer is one of the lowest for any cancer. Toll-like receptors (TLRs), evolutionarily conserved innate, are expressed in a wide variety of tissues and cell types, and they play key role in the innate immune system. TLRs have been found to be expressed by some kinds of tumor cells. However, what is the biological function of TLRs on tumor cells and whether human lung cancer cells can express TLRs remain to be fully understood. This review was performed to sum up the role of TLRs in lung cancer.     

Toll样受体信号通路的负调控

综述了Toll样受体(Toll-like receptors,TLRs)介导炎症反应信号通路的负调控机理．TLRs可以被病原体激活并迅速启动炎症反应,对先天性和获得性免疫反应起着重要调节作用．TLRs介导的免疫反应必须受到严格的调控,持续激活状态可长时间高表达炎症因子,导致机体产生慢性炎症、自身免疫紊乱和其他TLRs相关疾病．正常生理状态下,机体存在着多种TLRs的负调控机制,以维持免疫反应的平衡．该领域的研究近年来取得了重要进展,为许多免疫相关疾病的治疗提供了线索．