病原菌保守性特征分子及其介导的植物抗病性

每种病原菌都有一些保守的特征性分子,也称病原菌相关分子模式(PAMPs)。植物细胞表面的模式识别受体PRRs通过识别病原菌的PAMPs而激发免疫反应(PTI)。目前,已发现多种PRRs/PAMPs的识别模式,如拟南芥FLS2识别细菌鞭毛蛋白、拟南芥EFR识别细菌延长因子Tu(EF-Tu)、水稻CEBiP/CERK1识别真菌几丁质、水稻抗病蛋白XA21识别白叶枯病菌的硫化蛋白Ax21等。这些识别模式都能激发植物的基础免疫反应以抵抗病原菌的侵染。但是病原菌为了成功侵染寄主植物,也进化出一些致病机制,例如向植物细胞中注入毒性效应蛋白阻断PTI途径,或者产生一种"自我伪装"机制以逃避PRRs的识别。因此,研究者们根据PAMPs的结构特性对PRRs重新改造,以期使植物获得持久、广谱和高效的抗性。综述目前已知的PAMPs分子类型、PRRs/PAMPs的识别机制及改造后的新型PRRs,并分析PTI研究中存在的问题及其发展前景。     

Pattern recognition molecules and innate immunity to parasites

Recent pioneering advances in understanding how plants, insects and worms eliminate pathogens has led to the realization that innate immunity plays a vital role in protecting humans from infection. This comprehensive review examines the molecules involved in innate immune responses, how they act to control parasites and if their engagement can explain many immune features characteristic of parasitic infections.     

A novel fucose recognition fold involved in innate immunity

Anguilla anguilla agglutinin (AAA), a fucolectin found in the serum of European eel, participates in the recognition of bacterial liposaccharides by the animal innate immunity system. Because AAA specifically recognizes fucosylated terminals of H and Lewis (a) blood groups, it has been used extensively as a reagent in blood typing and histochemistry. AAA contains a newly discovered carbohydrate recognition domain present in proteins of organisms ranging from bacteria to vertebrates. The crystal structure of the complex of AAA with alpha-L-fucose characterizes the novel fold of this entire lectin family, identifying the residues that provide the structural determinants of oligosaccharide specificity. Modification of these residues explains how the different isoforms in serum can provide a diverse pathogen-specific recognition.     

Ubiquitination of pattern recognition receptors in plant innate immunity

Lacking an adaptive immune system, plants largely rely on plasma membrane‐resident pattern recognition receptors (PRRs) to sense pathogen invasion. The activation of PRRs leads to the profound immune responses that coordinately contribute to the restriction of pathogen multiplication. Protein post‐translational modifications dynamically shape the intensity and duration of the signalling pathways. In this review, we discuss the specific regulation of PRR activation and signalling by protein ubiquitination, endocytosis and degradation, with a particular focus on the bacterial flagellin receptor FLS2 (flagellin sensing 2) in Arabidopsis.     

Molecular battle between host and bacterium: recognition in innate immunity

During infection, our innate immune system is the first line of defense and has evolved to clear invading bacteria immediately. To do so, recognition is the key element. However, how does the innate immune system distinguish self from nonself, and how does it recognize all bacteria (estimated to be far over a million species)? The answer lies in the recognition of evolutionary conserved structures. In this review, we approach this phenomenon from the bacterial perspective. What are the evolutionary conserved structures in bacteria, and what strategies are there in the human innate immune system to sense these structures? We illustrate most examples both at the functional as well as at the molecular level. Furthermore, we highlight how pathogenic bacteria can evade this recognition to survive better in the human host which in turn can result in life‐threatening diseases. Copyright © 2011 John Wiley & Sons, Ltd.     

线粒体与固有免疫应答

线粒体是真核细胞至关重要的细胞器,在细胞生命周期中参与了很多关键进程,如ATP的供给、Ca2+动态平衡的维持、活性氧簇(Reactive oxygen species,ROS)的产生与清除、细胞凋亡等[1]。因此,不难想象,线粒体能够通过自身参与的各种生理     

cGLRs are a diverse family of pattern recognition receptors in innate immunity

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Peptidoglycan recognition proteins: a novel family of four human innate immunity pattern recognition molecules.

The innate immune system recognizes microorganisms through a series of pattern recognition receptors that are highly conserved in evolution. Insects have a family of 12 peptidoglycan recognition proteins (PGRPs) that recognize peptidoglycan, a ubiquitous component of bacterial cell walls. We report cloning of three novel human PGRPs (PGRP-L, PGRP-Ialpha, and PGRP-Ibeta) that together with the previously cloned PGRP-S, define a new family of human pattern recognition molecules. PGRP-L, PGRP-Ialpha, and PGRP-Ibeta have 576, 341, and 373 amino acids coded by five, seven, and eight exons on chromosomes 19 and 1, and they all have two predicted transmembrane domains. All mammalian and insect PGRPs have at least three highly conserved C-terminal PGRP domains located either in the extracellular or in the cytoplasmic (or in both) portions of the molecules. PGRP-L is expressed in liver, PGRP-Ialpha and PGRP-Ibeta in esophagus (and to a lesser extent in tonsils and thymus), and PGRP-S in bone marrow (and to a lesser extent in neutrophils and fetal liver). All four human PGRPs bind peptidoglycan and Gram-positive bacteria. Thus, these PGRPs may play a role in recognition of bacteria in these organs.     

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.     

Mitochondria and antiviral innate immunity

Mitochondria, dynamic organelles that undergo continuous cycles of fusion and fission, are the powerhouses of eukaryotic cells. Recent research indicates that mitochondria also act as platforms for antiviral immunity in vertebrates. Mitochondrial-mediated antiviral immunity depends on activation of the retinoic acid-inducible gene I (RIG-I)-like receptors signal transduction pathway and the participation of the mitochondrial outer membrane adaptor protein “mitochondrial antiviral signaling (MAVS)”. Here we discuss recent findings that suggest how mitochondria contribute to antiviral innate immunity.     

Autophagy and plant innate immunity

Plant innate immunity is often associated with specialized programmed cell death at or near the site of pathogen infection. Despite the isolation of several lesion mimic mutants, the molecular mechanisms that regulate cell death during an immune response remain obscure. Recently, autophagy, an evolutionarily conserved process of bulk protein and organelle turnover, was shown to play an important role in limiting cell death initiated during plant innate immune responses. Consistent with its role in plants, several studies in animals also demonstrate that the autophagic machinery is involved in innate as well as adaptive immunities. Here, we review the role of autophagy in plant innate immunity. Because autophagy is observed in healthy and dying plant cells, we will also examine whether autophagy plays a protective or a destructive role during an immune response.     

BVDV and innate immunity.

Infection with bovine viral diarrhea virus (BVDV) is prevalent in the cattle population worldwide. The virus exists in two biotypes, cytopathic and non-cytopathic, depending on the effect of the viruses on cultured cells. BVDV may cause transient and persistent infections which differ fundamentally in the host's antiviral immune response. Transient infection may be due to both cytopathic and non-cytopathic biotypes of BVDV and leads to a specific immune response. In contrast, only non-cytopathic BVD viruses can establish persistent infection as a result of infection of the embryo early in its development. Persistent infection is characterized by immunotolerance specific for the infecting viral strain. In this paper we discuss the role of innate immune responses in the two types of infection. In general, both transient and persistent infections are associated with an increased frequency of secondary infections. Associated with the increased risk of such infections are, among others, impaired bacteria killing and decreased chemotaxis. Interestingly, non-cytopathic BVDV fails to induce interferon type I in cultured bovine macrophages whereas cytopathic biotypes readily trigger this response. Cells infected with non-cytopathic BVDV are also resistant to induction of interferon by double stranded RNA, a potent interferon inducer signalling the presence of viral replication in the cell. Thus, non-cytopathic BVDV may dispose of a mechanism suppressing a key element of the antiviral defence of the innate immune system. Since interferon is also important in the activation of the adaptive immune response, suppression of this signal may be essential for the establishment of persistent infection and immunotolerance.     

Sugars and plant innate immunity

Sugars are involved in many metabolic and signalling pathways in plants. Sugar signals may also contribute to immune responses against pathogens and probably function as priming molecules leading to pathogen-associated molecular patterns (PAMP)-triggered immunity and effector-triggered immunity in plants. These putative roles also depend greatly on coordinated relationships with hormones and the light status in an intricate network. Although evidence in favour of sugar-mediated plant immunity is accumulating, more in-depth fundamental research is required to unravel the sugar signalling pathways involved. This might pave the way for the use of biodegradable sugar-(like) compounds to counteract plant diseases as cheaper and safer alternatives for toxic agrochemicals.