Role of LysM receptors in chitin-triggered plant innate immunity

Recent research findings clearly indicate that lysin motif (LysM)-containing cell surface receptors are involved in the recognition of specific oligosaccharide elicitors (chitin and peptidoglycan), which trigger an innate immunity response in plants. These receptors are either LysM-containing receptor-like kinases (LYKs) or LysM-containing receptor proteins (LYPs). In Arabidopsis, five LYKs (AtCERK1/AtLYK1 and AtLYK2–5) and three LYPs (AtLYP1–3) are likely expressed on the plasma membrane. In this review, we summarize recent research results on the role of these receptors in plant innate immunity, including the recent structural characterization of AtCERK1 and composition of the various receptor complexes in Arabidopsis.     

模式识别受体-Dectin-1的研究进展

Dectin-1是主要表达于髓样细胞中的非Toll样模式识别受体,它能诱导自身胞内信号介导一系列细胞反应,在抗真菌免疫中发挥着重要的作用.该文对Dectin-1介导的信号途径,Dectin-1与其他模式识别受体的相互作用,Dectin-1在适应性免疫、抗微生物免疫中的作用予以综述.     

System of innate immunity in plants

The review deals with the mechanisms of innate immunity in plants focusing on families of pattern-recognition receptors and incorporates recent data on complete sequencing of several plant genomes. Plant immune response involves several families of receptors, both membrane-bound and cytoplasmic ones, containing conservative leucine-rich repeats. The lack of adaptive immunity and the associated rearrangements in the immune receptor genes in plants is partly counterbalanced by genetically encoded mechanisms of specific immunity to particular pathogens. There is a certain similarity between intracellular signal transduction and effector mechanisms in plant and animal innate immune systems, although the latter are considerably more complex.     

Vesicle trafficking in plant immune responses

In plants, perception of pathogen-associated molecular patterns at the surface is the first line of defence in cellular immunity. This review summarizes recent evidence of the involvement of vesicle trafficking in the plant's immune response against pathogens. I first discuss aspects of ligand-stimulated receptor endocytosis. The best-characterized pattern-recognition receptor (PRR), FLS2, is a transmembrane leucine-rich repeat receptor kinase that recognizes bacterial flagellin. FLS2 was recently shown to undergo internalization upon activation with its cognate ligand. An animal PRR, TLR4 that mediates perception of bacterial-derived lipopolysaccharides, similarly exhibits ligand-stimulated endocytosis. The second focus is N-ethylmaleimide-sensitive factor adaptor protein receptor (SNARE)-mediated immunity involving syntaxins and their cognate partners. One of the genes involved in basal immunity in Arabidopsis, PEN1, encodes a syntaxin that focally accumulates at fungal penetration sites, raising the possibility that induced exocytosis is important for active defence. Pathogen-triggered endocytic and exocytic processes have to be balanced to ensure host cell homeostasis. Thus, understanding how phytopathogens have evolved strategies to exploit host cell vesicle trafficking to manipulate immune responses is currently an area of intense study.     

Cooperation of Toll-like receptor signals in innate immune defence

The mechanisms by which the recognition of Toll-like receptor (TLR) ligands leads to host immunity remain poorly defined. It is now thought that to induce an effective immune response, microorganisms must stimulate complex sets of pattern-recognition receptors, both within and outside of the TLR family. The combined activation of these different receptors can result in complementary, synergistic or antagonistic effects that modulate innate and adaptive immunity. Therefore, a complete understanding of the role of TLRs in host resistance to infection requires 'decoding' of these multiple receptor interactions. This Review highlights recent advances in the newly emerging field of TLR cooperation and discusses their implications for the development of adjuvants and immunotherapies.     

Th17 cells in immunity to Candida albicans

Our understanding of immunity to fungal pathogens has advanced considerably in recent years. Particularly significant have been the parallel discoveries in the C-type lectin receptor family and the Th effector arms of immunity, especially Th17 cells and their signature cytokine, IL-17. Many of these studies have focused on the most common human fungal pathogen, Candida albicans, which is typically a commensal microbe in healthy individuals but causes various disease manifestations in immunocompromised hosts, ranging from mild mucosal infections to lethal disseminated disease. Here, we discuss emerging fundamental discoveries with C.?albicans that have informed our overall molecular understanding of fungal immunity. In particular, we focus on the importance of pattern recognition receptor-mediated fungal recognition and subsequent IL-17 responses in host defense against mucosal candidiasis. In light of these recent advances, we also discuss the implications for anticytokine biologic therapy and vaccine development.     

CD14 signalling in lipid rafts: new ligands and co-receptors

PURPOSE OF REVIEW: Lipid rafts on monocytes/macrophages provide a dynamic microenvironment for an integrated lipopolysaccharide receptor (CD14)-dependent clustering of a set of receptors involved in innate immunity and clearance of atherogenic lipoproteins. The purpose of this review is to summarize the recent advances in our understanding of CD14-dependent receptor clustering and its relevance in atherogenesis. RECENT FINDINGS: Upon binding of various ligands, CD14 as a multiligand pattern recognition receptor induces specific coassembly of additional receptors present on circulating monocytes. SUMMARY: The composition of the receptor cluster and thus the associated signalling pathways defines a ligand specific cellular response, linking endogenous and exogenous host defense to a common recognition platform in rafts.     

Autophagy in antiviral innate immunity

Several autonomous arms of innate immunity help cells to combat viral infections. One of these is autophagy, a central cytosolic lysosomal‐dependent catabolic process constitutively competent to destroy infectious viruses as well as essential viral components that links virus detection to antiviral innate immune signals. Ongoing autophagy can be upregulated upon virus detection by pathogen receptors, including membrane bound and cytosolic pattern recognition receptors, and may further facilitate pattern recognition receptor‐dependent signalling. Autophagy or autophagy proteins also contribute to the synthesis of antiviral innate type I interferon cytokines as well as to antiviral interferon γ signalling. Additionally, autophagy may play a crucial role during viral infections in containing an excessive cellular response by regulating the intensity of the inflammatory response. As a consequence, viruses have evolved strategies to counteract antiviral innate immunity through manipulation of autophagy. This review highlights recent findings on the cross‐talk between autophagy and innate immunity during viral infections.     

T-cell activation: the power of one

Adaptive immunity depends on antigen-specific activation of resting lymphocytes. Using high-resolution live-cell imaging, a single ligand has been found to trigger a biochemical response in T cells. On the basis of this and other recent findings, a 'pseudodimer' with one foreign- and one self-antigen-engaged receptor linked via a CD4 molecule has been proposed as the fundamental unit of effective T-cell signaling.     

Role of the mannose receptor in the immune response

The mannose receptor (MR) recognizes a range of carbohydrates present on the surface and cell walls of micro-organisms. The MR is primarily expressed on macrophages and dendritic cells and is involved in MR-mediated endocytosis and phagocytosis. In addition, the MR plays a key role in host defense and provides a link between innate and adaptive immunity. Herein, we will review the role of the MR in innate host defense as well as the recent evidence for its role in the adaptive response, for both humoral and cellular immune responses.     

Cytokinin response induces immunity and fungal pathogen resistance,and modulates trafficking of the PRR LeEIX2 in tomato

Plant immunity is often defined by the immunity hormones: salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). These hormones are well known for differentially regulating defence responses against pathogens. In recent years, the involvement of other plant growth hormones such as auxin, gibberellic acid, abscisic acid, and cytokinins (CKs) in biotic stresses has been recognized. Previous reports have indicated that endogenous and exogenous CK treatment can result in pathogen resistance. We show here that CK induces systemic immunity in tomato (Solanum lycopersicum), modulating cellular trafficking of the pattern recognition receptor (PRR) LeEIX2, which mediates immune responses to Xyn11 family xylanases, and promoting resistance to Botrytis cinerea and Oidium neolycopersici in an SA- and ET-dependent mechanism. CK perception within the host underlies its protective effect. Our results support the notion that CK promotes pathogen resistance by inducing immunity in the host.     

Mechanisms of GII.4 norovirus evolution

Since the late 1990s norovirus (NoV) strains belonging to a single genotype (GII.4) have caused at least four global epidemics. To date, the higher epidemiological fitness of the GII.4 strains has been attributed to a faster rate of evolution within the virus capsid, resulting in the ability to escape herd immunity. Four key factors have been proposed to influence the rate of evolution in NoV. These include host receptor recognition, sequence space, duration of herd immunity, and replication kinetics. In this review we discuss recent advancements in our understanding of these four mechanisms in relation to GII.4 evolution.     

Phagosome as the organelle linking innate and adaptive immunity

The means by which phagocytosis and antimicrobial defense mechanisms are linked have expanded greatly in recent years. It is now clear that the process of phagocytosis does more than just degrade internalized microbes, but also helps coordinate the actions of the innate and adaptive immune system. This review will discuss the means by which Toll-like receptor signaling pathways are coordinated around the processes of phagocytosis, phagosome trafficking and autophagy and how these signaling pathways influence T-cell-mediated immunity. In this regard, we propose that at the subcellular level, phagosomes represent the smallest definable unit that links innate and adaptive immunity.     

Pattern recognition receptors: from the cell surface to intracellular dynamics

Detection of potentially infectious microorganisms is essential for plant immunity. Microbial communities growing on plant surfaces are constantly monitored according to their conserved microbe-associated molecular patterns (MAMPs). In recent years, several pattern-recognition receptors, including receptor-like kinases and receptor-like proteins, and their contribution to disease resistance have been described. MAMP signaling must be carefully controlled and seems to involve receptor endocytosis. As a further surveillance layer, plants are able to specifically recognize microbial effector molecules via nucleotide-binding site leucine-rich repeat receptors (NB-LRR). A number of recent studies show that NB-LRR translocate to the nucleus in order to exert their activity. In this review, current knowledge regarding the recognition of MAMPs by surface receptors, receptor activation, signaling, and subcellular redistribution are discussed.     

Role of pathogen's effectors in understanding host-pathogen interaction

Pathogens can pose challenges to plant growth and development at various stages of their life cycle. Two interconnected defense strategies prevent the growth of pathogens in plants, i.e., molecular patterns triggered immunity (PTI) and pathogenic effector-triggered immunity (ETI) that often provides resistance when PTI no longer functions as a result of pathogenic effectors. Plants may trigger an ETI defense response by directly or indirectly detecting pathogen effectors via their resistance proteins. A typical resistance protein is a nucleotide-binding receptor with leucine-rich sequences (NLRs) that undergo structural changes as they recognize their effectors and form associations with other NLRs. As a result of dimerization or oligomerization, downstream components activate “helper” NLRs, resulting in a response to ETI. It was thought that ETI is highly dependent on PTI. However, recent studies have found that ETI and PTI have symbiotic crosstalk, and both work together to create a robust system of plant defense. In this article, we have summarized the recent advances in understanding the plant's early immune response, its components, and how they cooperate in innate defense mechanisms. Moreover, we have provided the current perspective on engineering strategies for crop protection based on up-to-date knowledge.     

The role of Dectin-1 in the host defence against fungal infections

Dectin-1 is an innate immune pattern recognition receptor (PRR) that, through its ability to bind β-glucans, is involved in the recognition of several pathogenic fungi. Dectin-1 can stimulate a variety of cellular responses via the Syk/CARD9 signalling pathway, including phagocytosis, cytokine production and the respiratory burst. Several advances in our understanding of Dectin-1 immunobiology have been made in recent years, including characterisation of additional signalling pathways and demonstration of its ability to directly induce the development of adaptive immunity. However, the physiological role of many of the functions of this receptor is still unclear. This review aims to provide an update on Dectin-1 and its role within antifungal immune responses, focussing on progress made in the last two years.     

CD19-CD21 complex regulates an intrinsic Src family kinase amplification loop that links innate immunity with B-lymphocyte intracellular calcium responses

CD19 is a B-lymphocyte cell surface molecule that functions as a general response regulator or rheostat, which defines intrinsic and B-cell antigen receptor-induced signalling thresholds that are critical for humoral immunity and expansion of the peripheral B-cell pool. In addition, B-cell responses are influenced by signals transduced through a CD19-CD21 cell surface receptor complex, where the binding of complement C3d to CD21 links humoral immune responses with the innate immune system. This review outlines recent biochemical and genetic studies that characterize the signal transduction pathways utilized by this receptor complex to regulate B-cell intracellular calcium responses.     

Intracellular recognition of pathogens and autophagy as an innate immune host defence

Pathogen recognition is the first and crucial step in innate immunity. Molecular families involved in the recognition of pathogens and activation of the innate immune responses in immunoreactive cells include the Toll-like receptor family in mammals and the peptidoglycan recognition protein (PGRP) family in Drosophila, which sense microorganisms in an extracellular or luminal compartment. Other emerging families are the intracellular recognition molecules for bacteria, such as nucleotide binding and oligomerization domain-like receptors in mammals and PGRP--LE in Drosophila, several of which have been shown to detect structures of bacterial peptidoglycan in the host cell cytosol. Exciting advances in recent studies on autophagy indicate that macroautophagy (referred to here as autophagy) is selectively induced by intracellular recognition molecules and has a crucial role in the elimination of intracellular pathogens, including bacteria, viruses and parasites. This review discusses recent studies related to intracellular recognition molecules and innate immune responses to intracellular pathogens, and highlights the role of autophagy in innate immunity.     

Coordinated Neutralization and Immune Activation by the Cytosolic Antibody Receptor TRIM21

TRIM21 is a high-affinity antibody receptor uniquely expressed in the cytosol of mammalian cells. Here we summarize its role in extending antibody protection into the intracellular environment and allowing nonprofessional cells to benefit from adaptive immunity. We highlight recent work that has shed light on how TRIM21 acts as both an immune sensor and effector. We also review how TRIM21 synergizes with other innate immune receptors to promote an integrated antiviral response.     

Roles of ubiquitination in pattern-recognition receptors and type I interferon receptor signaling

Post-translational protein modifications are involved in all functions of living cells. This includes the ability of cells to recognize pathogens and regulate genes involved in their clearance, a concept known as innate immunity. While phosphorylation mechanisms play essential roles in regulating different aspects of the innate immune response, ubiquitination is now recognized as another post-translational modification that works in parallel with phosphorylation to orchestrate the final proper innate immune response against invading pathogens. More precisely, this review will discuss the most recent advances that address the role of ubiquitination in pattern-recognition receptors and type I interferon receptor signaling.