Toll样受体在寄生虫感染过程中的作用

Toll样受体（TLR）是天然免疫系统识别病原微生物的主要受体,在天然免疫反应中具有重要的作用。TLR通过识别病原相关模式分子以激活抗感染的天然免疫应答和适应性免疫应答。TLR信号通路可通过诱导炎性因子的产生在适应性免疫应答中发挥重要作用。本文就TLR在寄生虫感染中发挥的作用作一综述。     

TLR7介导抗病毒免疫应答研究进展

Toll样受体（Toll-like receptors，TLRs）是天然免疫中重要的模式识别受体，在机体抗病原体感染中发挥重要的作用，同时也是连接天然免疫与获得性免疫的桥梁。研究表明，Toll样受体7（TLR7）能识别某些小分子的抗病毒化合物和病毒单链RNA（single-stranded RNA，ssRNA），活化的TLR7启动髓系分化因子88（myeloid differentiation factor88，MyD88）依赖的信号通路，介导抗病毒免疫应答。TLR7的活化需要内体，溶酶体的成熟，目前一些小分子的TLR7配体已用于临床治疗病毒性感染疾病和肿瘤。     

Toll样受体3在病毒感染及细胞凋亡中的生物学功能

Toll样受体3（TLR3）作?《舅碦NA识别受体在机体抗病毒天然免疫中发挥十分重要的作用。TLR3识别配体后通过含TIR结构域的转接蛋白（TRIF）途径活化转录因子NF-κB和干扰素调节因子3（IRF3）,诱导炎症细胞释放炎症因子并介导炎症反应,同时诱导I型干扰素的释放,介导抗病毒天然免疫。在一些病毒感染中TLR3通过诱导组织损伤介导病毒的扩散从而加重疾病的严重程度。部分肿瘤细胞也表达TLR3,活化的TLR3介导细胞凋亡、抑制细胞增殖,提示TLR3可能是肿瘤免疫治疗的新靶点。［关键词］ Toll样受体3;信号转导;病毒;肿瘤;细胞凋亡     

Dectin-1与非Toll样模式识别受体免疫识别的研究进展

Toll样受体（TLR）是一类天然免疫相关的模式识别受体（PRR），在机体抵御感染中发挥着极为重要的作用。除TLR外，目前还发现了很多其它种类PRR，这些非Toll样PRR在天然免疫中的作用也是不可缺少的，它们既可以与TLR协同作用，也可以单独发挥作用。Dectin-1是近年来颇受关注的一种非Toll样PRR，属于NK细胞受体样C型凝集素，是一种Ⅱ型跨膜受体，通过对真菌的识别参与免疫效应细胞的吞噬及杀伤过程，诱导机体产生一系列的细胞因子及趋化因子，从而参与机体防御真菌病原体的天然免疫反应，但在某些情况下也可能引起自身免疫性疾病的发生。     

人Toll样受体9基因多态性与免疫异常疾病的相关性研究进展

Toll样受体9（TLR9）是一种模式识别受体,在天然免疫系统及获得性免疫应答的激活和调节中发挥着重要作用。TLR9基因被认为是炎性相关基因,基因的变异可能与许多免疫异常疾病有相关性,主要包括Th-2驱使的特异反应性疾病及以Th-1占主体的自身免疫性疾病。国内外已有许多关于人TLR9基因多态性与免疫异常疾病易感性的研究,该文就这些研究作一综述。     

Tol1样受体—一个新发现的介导天然免疫的古老家族(下)

在前文基础上 ,介绍了Toll样受体家族重要成员TLR2、TLR4的配体 ;LPS与TLR2、TLR4的相互作用 ;归纳了Toll样受体的免疫学意义。它是迄今认识的第一个机体通过感知微生物病原体直接作出防御反应的天然免疫受体。Toll样受体的发现和功能研究为了解与感染有关的免疫现象 ,如炎症、自身免疫病、天然免疫与获得免疫的关系等 ,提供了深入思考的素材     

TLR7介导抗病毒免疫应答研究进展

Toll样受体(Toll-like receptors,TLRs)是天然免疫中重要的模式识别受体,在机体抗病原体感染中发挥重要的作用,同时也是连接天然免疫与获得性免疫的桥梁。研究表明,Toll样受体7(TLR7)能识别某些小分子的抗病毒化合物和病毒单链RNA(single-stranded RNA,ssRNA),活化的TLR7启动髓系分化因子88(myeloid differentiation factor 88,MyD88)依赖的信号通路,介导抗病毒免疫应答。TLR7的活化需要内体/溶酶体的成熟,目前一些小分子的TLR7配体已用于临床治疗病毒性感染疾病和肿瘤。     

025 Toll样受体-一个新发现的介导天然免疫的古老家族(下)

在前文基础上,介绍了Toll样受体家族重要成员TLR2、TLR4的配体;LPS与TLR2、TLR4的相互作用;归纳了Toll样受体的免疫学意义.它是迄今认识的第一个机体通过感知微生物病原体直接作出防御反应的天然免疫受体.Toll样受体的发现和功能研究为了解与感染有关的免疫现象,如炎症、自身免疫病、天然免疫与获得免疫的关系等,提供了深入思考的素材.     

调节免疫反应的CpG-ODN

Toll样受体(TLR)最初被认为在识别病原和激活天然免疫中发挥重要作用,现在发现通过活化TLR可以调节天然免疫和适应性免疫反应。在很多研究中,TLR-9的配体CpG-ODN引起了人们广泛的兴趣,其重要原因之一就是CpG-ODN容易人工合成和进行各种修饰以改变其免疫刺激活性。现在CpG-ODN的研究已从基础研究逐步向临床药物开发方向发展。     

Toll样受体3介导抑制Bewo细胞中乙型肝炎病毒复制

目的探讨Toll样受体3（TLR3）介导的天然免疫对Bewo细胞中乙型肝炎病毒（HBV）复制的影响。方法首先用TLR3配体polyI：C处理Bewo细胞,观察细胞TLR3 mRNA表达的动力学。然后将2μg 1.3倍HBV全基因重组质粒pcDNA3.1（＋）-HBV1.3转染Bewo细胞,12h后,以polyI：C处理3d。最后,用抗TLR3处理Bewo细胞1h后,加入25μg/ml polyI：C刺激。采用荧光定量RT-PCR、微粒子酶免疫分析法（MEIA）和荧光定量PCR法分别检测细胞TLR3mRNA表达、HBsAg、HBeAg及HBV DNA水平。结果 polyI：C可显著诱导Bewo细胞TLR3 mRNA表达（P〈0.05）,呈时间和剂量依赖性;与对照组比较,polyI：C可显著抑制HBV复制（P〈0.001）,抗TLR3可显著逆转polyI：C对HBV复制的抑制作用（P〈0.01）。结论 TLR3介导的天然免疫能一定程度抑制Bewo细胞中HBV复制,为防治HBV宫内感染提供了新的途径。     

TLR4与中枢神经系统损伤

As a receptor mediating the transmembrane signal transduction in the innate immunity, Toll-like receptor 4 (TLR4) is a bridge between innate immunity and required immunity, and plays an important role when signal-transducing of some cells are activated. Recent reports show that TLR4 expresses in the different glial cells and strongly links to the innate immune activation and inflammatory response in the central nervous system (CNS). TLR4 plays a key role in the processes of brain damage by infection of the CNS, stroke, cerebral hemorrhage and trauma. In this review, we concentrate on recent findings regarding the progress of function and mechanism of TLR4 in the processes of the CNS damage in various diseases.     

Natural killer cells: versatile roles in autoimmune and infectious diseases

Natural killer (NK) cells are essential members of innate immunity and they rapidly respond to a variety of insults via cytokine secretion and cytolytic activity. Effector functions of NK cells form an important first line of innate immunity against viral, bacterial and parasitic infections, as well as an important bridge for the activation of adaptive immune responses. The control of NK-cell activation and killing is now understood to be a highly complex system of diverse inhibitory and activatory receptor–ligand interactions, sensing changes in MHC expression. NK cells have a functional role in innate immunity as the primary source of NK-cell-derived immunoregulatory cytokines, which have been identified in target organs of patients suffering from autoimmune diseases, and play a critical role in early defense against infectious agents. This review focuses on recent research of NK cells, summarizing their potential immunoregulatory role in modulating autoimmunity and infectious diseases.     

Toll样受体调节中性粒细胞免疫作用的研究进展

Toll样受体（TLR）是固有免疫系统中特异的I型跨膜受体及病原模式识别受体。TLR能特异地识别病原体相关分子模式（PAMP）,构成机体抵御病原微生物的第一道防线,因而在固有免疫系统中发挥重要作用,而且TLR还能调节适应性免疫,是连接固有免疫和适应性免疫的桥梁。中性粒细胞（PMN）是机体最重要的炎性细胞,在固有免疫中扮演着十分重要的角色,对炎症的发生、发展及转归起了关键的作用。作为重要受体的TLR能诱导PMN的生存与活化,在急性炎症反应、细胞信号转导和细胞凋亡中起着重要作用。     

Role of HLA-G in innate immunity through direct activation of NF-kappaB in natural killer cells

HLA-G is a non-classical HLA class I molecule involved in immunotolerance. HLA-G protects the fetus from maternal immune recognition and promotes allograft acceptance and tumor escape. Its low polymorphism and primary function, which is not peptide presentation to T lymphocytes, led us to compare the signal transduced after interaction between HLA-G and its receptor to those of innate immunity receptors with their ligands. We investigated the role of HLA-G in the classical NF-kappaB pathway in natural killer (NK) cells, which is the major pathway activated by innate immunity receptors. In NK cells stimulated with HLA-G1-expressed cells, we demonstrate that HLA-G induces the phosphorylation and the degradation of IkappaBalpha leading to nuclear translocation of NF-kappaB. This effect is independent of the presence of ILT-2 receptors and is still observed using a peptide corresponding to the alpha-1 domain of HLA-G. All these data support an unsuspected role for HLA-G in innate immunity by activating classical NF-kappaB pathway in NK cells.     

Role of Innate Immunity in the Pathogenesis of Type 1 and Type 2 Diabetes

The importance of innate immunity in host defense is becoming clear after discovery of innate immune receptors such as Toll-like receptor or Nod-like receptor. Innate immune system plays an important role in diverse pathological situations such as autoimmune diseases. Role of innate immunity in the pathogenesis of metabolic disorders such as type 2 diabetes, metabolic syndrome or atherosclerosis that has not been previously considered as inflammatory disorders, is also being appreciated. Here, the role of innate immunity in the development of type 1 diabetes, a classical organ-specific autoimmune disease, and type 2 diabetes will be discussed, focusing on the role of specific innate immune receptors involved in these disease processes.

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IRAK-4--a shared NF-kappaB activator in innate and acquired immunity

The human body is protected against external pathogens by two immune systems: innate and acquired immunities. Whereas innate immunity exhibits immediate responses to external pathogens by recognizing pathogen-associated molecular patterns (PAMPs), adaptive immunity uses T cells to recognize and defend against pathogens by developing effector cells, antibodies and memory cells. Although each system seems to possess distinct activation mechanisms, interleukin-1 receptor-associated kinase (IRAK)-4 is essential for NF-kappaB activation in Toll-like receptor (TLR) and T-cell receptor (TCR) signaling pathways. This implies possible crosstalk between innate and acquired immunities, and evolutionary development that resulted in the use of innate signaling molecules by the acquired immune system. Here, we discuss the impact of these evolutionarily conserved molecules on innate and acquired immunity, and their potential as drug targets for the simultaneous modulation of both immunities.     

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Trained immunity from the perspective of Plasmodium infection

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