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1

Witzell, Johanna, and Juan A. Martín. "Phenolic metabolites in the resistance of northern forest trees to pathogens — past experiences and future prospects." Canadian Journal of Forest Research 38, no. 11 (November 2008): 2711–27. http://dx.doi.org/10.1139/x08-112.

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Phenolic metabolites are frequently implicated in chemical defense mechanisms against pathogens in woody plants. However, tree breeding programmes for resistance to pathogens and practical tree-protection applications based on these compounds seem to be scarce. To identify gaps in our current knowledge of this subject, we explored some of the recent literature on the involvement of phenolic metabolites in the resistance of northern forest trees (Pinus, Picea, Betula, Populus, and Salix spp.) to pathogens. Although it is evident that the phenolic metabolism of trees is often activated by pathogen attacks, few studies have convincingly established that this induction is due to a specific defense response that is capable of stopping the invading pathogen. The role of constitutive phenolics in the resistance of trees to pathogens has also remained unclear. In future studies, the importance of phenolics in oxidative stress, cell homeostasis and tolerance, and the spatial and temporal localization of phenolics in relation to invading pathogens should be more carefully acknowledged. Possibilities for future studies using advanced methods (e.g., metabolic profiling, confocal laser scanning microscopy, and use of modified tree genotypes) are discussed.
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2

Mastellos, Dimitrios, and John D. Lambris. "Complement: more than a ‘guard’ against invading pathogens?" Trends in Immunology 23, no. 10 (October 2002): 485–91. http://dx.doi.org/10.1016/s1471-4906(02)02287-1.

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3

Islam, Waqar, Muhammad Qasim, Ali Noman, Muhammad Adnan, Muhammad Tayyab, Taimoor Hassan Farooq, Huang Wei, and Liande Wang. "Plant microRNAs: Front line players against invading pathogens." Microbial Pathogenesis 118 (May 2018): 9–17. http://dx.doi.org/10.1016/j.micpath.2018.03.008.

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4

Akira, Shizuo. "Innate immunity and adjuvants." Philosophical Transactions of the Royal Society B: Biological Sciences 366, no. 1579 (October 12, 2011): 2748–55. http://dx.doi.org/10.1098/rstb.2011.0106.

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Innate immunity was for a long time considered to be non-specific because the major function of this system is to digest pathogens and present antigens to the cells involved in acquired immunity. However, recent studies have shown that innate immunity is not non-specific, but is instead sufficiently specific to discriminate self from pathogens through evolutionarily conserved receptors, designated Toll-like receptors (TLRs). Indeed, innate immunity has a crucial role in early host defence against invading pathogens. Furthermore, TLRs were found to act as adjuvant receptors that create a bridge between innate and adaptive immunity, and to have important roles in the induction of adaptive immunity. This paradigm shift is now changing our thinking on the pathogenesis and treatment of infectious, immune and allergic diseases, as well as cancers. Besides TLRs, recent findings have revealed the presence of a cytosolic detector system for invading pathogens. I will review the mechanisms of pathogen recognition by TLRs and cytoplasmic receptors, and then discuss the roles of these receptors in the development of adaptive immunity in response to viral infection.
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5

DUCROT, ARNAUD, and MICHEL LANGLAIS. "TRAVELLING WAVES IN INVASION PROCESSES WITH PATHOGENS." Mathematical Models and Methods in Applied Sciences 18, no. 03 (March 2008): 325–49. http://dx.doi.org/10.1142/s021820250800270x.

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This work is devoted to the study of a singular reaction–diffusion system arising in modelling the introduction of a lethal pathogen within an invading host population. In the absence of the pathogen, the host population exhibits a bistable dynamics (or Allee effect). Earlier numerical simulations of the singular SI model under consideration have exhibited stable travelling waves and also, under some circumstances, a reversal of the wave front speed due to the introduction of the pathogen. Here we prove the existence of such travelling wave solutions, study their linear stability and give analytical conditions yielding a reversal of the wave front speed, i.e. the invading host population may eventually retreat following the introduction of the lethal pathogen.
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6

Qiao, Yongli, Rui Xia, Jixian Zhai, Yingnan Hou, Li Feng, Yi Zhai, and Wenbo Ma. "Small RNAs in Plant Immunity and Virulence of Filamentous Pathogens." Annual Review of Phytopathology 59, no. 1 (August 25, 2021): 265–88. http://dx.doi.org/10.1146/annurev-phyto-121520-023514.

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Gene silencing guided by small RNAs governs a broad range of cellular processes in eukaryotes. Small RNAs are important components of plant immunity because they contribute to pathogen-triggered transcription reprogramming and directly target pathogen RNAs. Recent research suggests that silencing of pathogen genes by plant small RNAs occurs not only during viral infection but also in nonviral pathogens through a process termed host-induced gene silencing, which involves trans-species small RNA trafficking. Similarly, small RNAs are also produced by eukaryotic pathogens and regulate virulence. This review summarizes the small RNA pathways in both plants and filamentous pathogens, including fungi and oomycetes, and discusses their role in host–pathogen interactions. We highlight secondarysmall interfering RNAs of plants as regulators of immune receptor gene expression and executors of host-induced gene silencing in invading pathogens. The current status and prospects of trans-species gene silencing at the host–pathogen interface are discussed.
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7

Cipriano, Michael J., and Stephen L. Hajduk. "Drivers of persistent infection: pathogen-induced extracellular vesicles." Essays in Biochemistry 62, no. 2 (April 17, 2018): 135–47. http://dx.doi.org/10.1042/ebc20170083.

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Extracellular vesicles (EVs) are produced by invading pathogens and also by host cells in response to infection. The origin, composition, and function of EVs made during infection are diverse and provide effective vehicles for localized and broad dissimilation of effector molecules in the infected host. Extracellular pathogens use EVs to communicate with each other by sensing the host environment contributing to social motility, tissue tropism, and persistence of infection. Pathogen-derived EVs can also interact with host cells to influence the adhesive properties of host membranes and to alter immune recognition and response. Intracellular pathogens can affect both the protein and RNA content of EVs produced by infected host cells. Release of pathogen-induced host EVs can affect host immune responses to infection. In this review, we will describe both the biogenesis and content of EVs produced by a number of diverse pathogens. In addition, we will examine the pathogen-induced changes to EVs produced by infected host cells.
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8

Slimmen, Lisa J. M., Hettie M. Janssens, Annemarie M. C. van Rossum, and Wendy W. J. Unger. "Antigen-Presenting Cells in the Airways: Moderating Asymptomatic Bacterial Carriage." Pathogens 10, no. 8 (July 28, 2021): 945. http://dx.doi.org/10.3390/pathogens10080945.

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Bacterial respiratory tract infections (RTIs) are a major global health burden, and the role of antigen-presenting cells (APCs) in mounting an immune response to contain and clear invading pathogens is well-described. However, most encounters between a host and a bacterial pathogen do not result in symptomatic infection, but in asymptomatic carriage instead. The fact that a pathogen will cause infection in one individual, but not in another does not appear to be directly related to bacterial density, but rather depend on qualitative differences in the host response. Understanding the interactions between respiratory pathogens and airway APCs that result in asymptomatic carriage, will provide better insight into the factors that can skew this interaction towards infection. This review will discuss the currently available knowledge on airway APCs in the context of asymptomatic bacterial carriage along the entire respiratory tract. Furthermore, in order to interpret past and futures studies into this topic, we propose a standardized nomenclature of the different stages of carriage and infection, based on the pathogen’s position with regard to the epithelium and the amount of inflammation present.
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9

Hendricks, Matthew R., and Jennifer M. Bomberger. "Who's really in control: microbial regulation of protein trafficking in the epithelium." American Journal of Physiology-Cell Physiology 306, no. 3 (February 1, 2014): C187—C197. http://dx.doi.org/10.1152/ajpcell.00277.2013.

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Due to evolutionary pressure, there are many complex interactions at the interface between pathogens and eukaryotic host cells wherein host cells attempt to clear invading microorganisms and pathogens counter these mechanisms to colonize and invade host tissues. One striking observation from studies focused on this interface is that pathogens have multiple mechanisms to modulate and disrupt normal cellular physiology to establish replication niches and avoid clearance. The precision by which pathogens exert their effects on host cells makes them excellent tools to answer questions about cell physiology of eukaryotic cells. Furthermore, an understanding of these mechanisms at the host-pathogen interface will benefit our understanding of how pathogens cause disease. In this review, we describe a few examples of how pathogens disrupt normal cellular physiology and protein trafficking at epithelial cell barriers to underscore how pathogens modulate cellular processes to cause disease and how this knowledge has been utilized to learn about cellular physiology.
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10

Perry, William J., Jeffrey M. Spraggins, Jessica R. Sheldon, Caroline M. Grunenwald, David E. Heinrichs, James E. Cassat, Eric P. Skaar, and Richard M. Caprioli. "Staphylococcus aureus exhibits heterogeneous siderophore production within the vertebrate host." Proceedings of the National Academy of Sciences 116, no. 44 (October 14, 2019): 21980–82. http://dx.doi.org/10.1073/pnas.1913991116.

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Siderophores, iron-scavenging small molecules, are fundamental to bacterial nutrient metal acquisition and enable pathogens to overcome challenges imposed by nutritional immunity. Multimodal imaging mass spectrometry allows visualization of host−pathogen iron competition, by mapping siderophores within infected tissue. We have observed heterogeneous distributions of Staphylococcus aureus siderophores across infectious foci, challenging the paradigm that the vertebrate host is a uniformly iron-depleted environment to invading microbes.
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11

Falsig, Jeppe, Johan van Beek, Corinna Hermann, and Marcel Leist. "Molecular basis for detection of invading pathogens in the brain." Journal of Neuroscience Research 86, no. 7 (2008): 1434–47. http://dx.doi.org/10.1002/jnr.21590.

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12

Górski, Andrzej, and Beata Weber-Dabrowska. "The potential role of endogenous bacteriophages in controlling invading pathogens." Cellular and Molecular Life Sciences 62, no. 5 (March 2005): 511–19. http://dx.doi.org/10.1007/s00018-004-4403-6.

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13

Parnell, S., T. R. Gottwald, T. Riley, and F. van den Bosch. "A generic risk-based surveying method for invading plant pathogens." Ecological Applications 24, no. 4 (June 2014): 779–90. http://dx.doi.org/10.1890/13-0704.1.

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14

Kim, Byoung Sik. "Spatiotemporal Regulation of Vibrio Exotoxins by HlyU and Other Transcriptional Regulators." Toxins 12, no. 9 (August 22, 2020): 544. http://dx.doi.org/10.3390/toxins12090544.

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After invading a host, bacterial pathogens secrete diverse protein toxins to disrupt host defense systems. To ensure successful infection, however, pathogens must precisely regulate the expression of those exotoxins because uncontrolled toxin production squanders energy. Furthermore, inappropriate toxin secretion can trigger host immune responses that are detrimental to the invading pathogens. Therefore, bacterial pathogens use diverse transcriptional regulators to accurately regulate multiple exotoxin genes based on spatiotemporal conditions. This review covers three major exotoxins in pathogenic Vibrio species and their transcriptional regulation systems. When Vibrio encounters a host, genes encoding cytolysin/hemolysin, multifunctional-autoprocessing repeats-in-toxin (MARTX) toxin, and secreted phospholipases are coordinately regulated by the transcriptional regulator HlyU. At the same time, however, they are distinctly controlled by a variety of other transcriptional regulators. How this coordinated but distinct regulation of exotoxins makes Vibrio species successful pathogens? In addition, anti-virulence strategies that target the coordinating master regulator HlyU and related future research directions are discussed.
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15

Ashrafi, Nadia, Cristian Lapthorn, Frank S. Pullen, Fernando Naclerio, and Birthe V. Nielsen. "High performance liquid chromatography coupled to electrospray ionisation mass spectrometry method for the detection of salivary human neutrophil alpha defensins HNP1, HNP2, HNP3 and HNP4." Analytical Methods 9, no. 46 (2017): 6482–90. http://dx.doi.org/10.1039/c7ay01676j.

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16

Kyrklund, Mikael, Heidi Kaski, Ramin Akhi, Antti E. Nissinen, Outi Kummu, Ulrich Bergmann, Pirkko Pussinen, Sohvi Hörkkö, and Chunguang Wang. "Existence of natural mouse IgG mAbs recognising epitopes shared by malondialdehyde acetaldehyde adducts and Porphyromonas gingivalis." Innate Immunity 27, no. 2 (January 14, 2021): 158–69. http://dx.doi.org/10.1177/1753425920981133.

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Natural Abs are produced by B lymphocytes in the absence of external Ag stimulation. They recognise self, altered self and foreign Ags, comprising an important first-line defence against invading pathogens and serving as innate recognition receptors for tissue homeostasis. Natural IgG Abs have been found in newborns and uninfected individuals. Yet, their physiological role remains unclear. Previously, no natural IgG Abs to oxidation-specific epitopes have been reported. Here, we show the cloning and characterisation of mouse IgG mAbs against malondialdehyde acetaldehyde (MAA)-modified low-density lipoprotein. Sequence analysis reveals high homology with germline genes, suggesting that they are natural. Further investigation shows that the MAA-specific natural IgG Abs cross-react with the major periodontal pathogen Porphyromonas gingivalis and recognise its principle virulence factors gingipain Kgp and long fimbriae. The study provides evidence that natural IgGs may play an important role in innate immune defence and in regulation of tissue homeostasis by recognising and removing invading pathogens and/or modified self-Ags, thus being involved in the development of periodontitis and atherosclerosis.
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17

Danastas, Kevin, Monica Miranda-Saksena, and Anthony L. Cunningham. "Herpes Simplex Virus Type 1 Interactions with the Interferon System." International Journal of Molecular Sciences 21, no. 14 (July 21, 2020): 5150. http://dx.doi.org/10.3390/ijms21145150.

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The interferon (IFN) system is one of the first lines of defense activated against invading viral pathogens. Upon secretion, IFNs activate a signaling cascade resulting in the production of several interferon stimulated genes (ISGs), which work to limit viral replication and establish an overall anti-viral state. Herpes simplex virus type 1 is a ubiquitous human pathogen that has evolved to downregulate the IFN response and establish lifelong latent infection in sensory neurons of the host. This review will focus on the mechanisms by which the host innate immune system detects invading HSV-1 virions, the subsequent IFN response generated to limit viral infection, and the evasion strategies developed by HSV-1 to evade the immune system and establish latency in the host.
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18

Sheldon, I. Martin, James G. Cronin, and John J. Bromfield. "Tolerance and Innate Immunity Shape the Development of Postpartum Uterine Disease and the Impact of Endometritis in Dairy Cattle." Annual Review of Animal Biosciences 7, no. 1 (February 15, 2019): 361–84. http://dx.doi.org/10.1146/annurev-animal-020518-115227.

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Bacteria are ubiquitous in the bovine uterus after parturition, but 50 years ago, cows tolerated these bacteria and few animals developed uterine disease. Now, up to 40% of dairy cattle develop postpartum uterine disease. Uterine disease causes infertility by compromising the function of not only the endometrium but also the ovary. Animals defend themselves against pathogens using tolerance and resistance mechanisms. Tolerance is the ability to limit the disease severity induced by a given pathogen burden. Resistance is the ability to limit the pathogen burden and is usually the function of immunity. Endometrial cells contribute to tolerance and have roles in innate immunity and the inflammatory response to pathogens. However, failures in endometrial tolerance and the character of the inflammatory response shape postpartum uterine disease. We propose that uterine health is more dependent on the ability of the endometrium to tolerate pathogens than the ability to resist invading bacteria.
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19

Aliberti, Julio. "Immunity and Tolerance Induced by Intestinal Mucosal Dendritic Cells." Mediators of Inflammation 2016 (2016): 1–8. http://dx.doi.org/10.1155/2016/3104727.

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Dendritic cells present in the digestive tract are constantly exposed to environmental antigens, commensal flora, and invading pathogens. Under steady-state conditions, these cells have high tolerogenic potential, triggering differentiation of regulatory T cells to protect the host from unwanted proinflammatory immune responses to innocuous antigens or commensals. On the other hand, these cells must discriminate between commensal flora and invading pathogens and mount powerful immune response against pathogens. A potential result of unbalanced tolerogenic versus proinflammatory responses mediated by dendritic cells is associated with chronic inflammatory conditions, such as Crohn’s disease, ulcerative colitis, food allergies, and celiac disease. Herein, we review the dendritic cell population involved in mediating tolerance and immunity in mucosal surfaces, the progress in unveiling their development in vivo, and factors that can influence their functions.
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20

Nouwen, Lonneke V., and Bart Everts. "Pathogens MenTORing Macrophages and Dendritic Cells: Manipulation of mTOR and Cellular Metabolism to Promote Immune Escape." Cells 9, no. 1 (January 9, 2020): 161. http://dx.doi.org/10.3390/cells9010161.

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Myeloid cells, including macrophages and dendritic cells, represent an important first line of defense against infections. Upon recognition of pathogens, these cells undergo a metabolic reprogramming that supports their activation and ability to respond to the invading pathogens. An important metabolic regulator of these cells is mammalian target of rapamycin (mTOR). During infection, pathogens use host metabolic pathways to scavenge host nutrients, as well as target metabolic pathways for subversion of the host immune response that together facilitate pathogen survival. Given the pivotal role of mTOR in controlling metabolism and DC and macrophage function, pathogens have evolved strategies to target this pathway to manipulate these cells. This review seeks to discuss the most recent insights into how pathogens target DC and macrophage metabolism to subvert potential deleterious immune responses against them, by focusing on the metabolic pathways that are known to regulate and to be regulated by mTOR signaling including amino acid, lipid and carbohydrate metabolism, and autophagy.
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21

Hardham, Adrienne R., and David M. Cahill. "The role of oomycete effectors in plant - pathogen interactions." Functional Plant Biology 37, no. 10 (2010): 919. http://dx.doi.org/10.1071/fp10073.

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Plants constantly come into contact with a diverse range of microorganisms that are potential pathogens, and they have evolved multi-faceted physical and chemical strategies to inhibit pathogen ingress and establishment of disease. Microbes, however, have developed their own strategies to counteract plant defence responses. Recent research on plant–microbe interactions has revealed that an important part of the infection strategies of a diverse range of plant pathogens, including bacteria, fungi and oomycetes, is the production of effector proteins that are secreted by the pathogen and that promote successful infection by manipulating plant structure and metabolism, including interference in plant defence mechanisms. Pathogen effector proteins may function either in the extracellular spaces within plant tissues or within the plant cell cytoplasm. Extracellular effectors include cell wall degrading enzymes and inhibitors of plant enzymes that attack invading pathogens. Intracellular effectors move into the plant cell cytoplasm by as yet unknown mechanisms where, in incompatible interactions, they may be recognised by plant resistance proteins but where, in compatible interactions, they may suppress the plant’s immune response. This article presents a brief overview of our current understanding of the nature and function of effectors produced by oomycete plant pathogens.
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22

Sharp, Ryan T., Michael W. Shaw, and Frank Bosch. "The effect of competition on the control of invading plant pathogens." Journal of Applied Ecology 57, no. 7 (April 17, 2020): 1403–12. http://dx.doi.org/10.1111/1365-2664.13618.

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23

Thompson, Robin N., Christopher A. Gilligan, and Nik J. Cunniffe. "Control fast or control smart: When should invading pathogens be controlled?" PLOS Computational Biology 14, no. 2 (February 16, 2018): e1006014. http://dx.doi.org/10.1371/journal.pcbi.1006014.

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24

Carella, Philip. "Resistance on Tap: PDR Transporters Direct Antimicrobial Metabolites Toward Invading Pathogens." Plant Cell 31, no. 9 (July 2, 2019): 1943–44. http://dx.doi.org/10.1105/tpc.19.00470.

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25

Prolo, Carolina, María Noel Álvarez, and Rafael Radi. "Peroxynitrite, a potent macrophage-derived oxidizing cytotoxin to combat invading pathogens." BioFactors 40, no. 2 (November 26, 2013): 215–25. http://dx.doi.org/10.1002/biof.1150.

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26

Sun, Lixiang, Wenjie Liu, and Ling-juan Zhang. "The Role of Toll-Like Receptors in Skin Host Defense, Psoriasis, and Atopic Dermatitis." Journal of Immunology Research 2019 (November 14, 2019): 1–13. http://dx.doi.org/10.1155/2019/1824624.

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As the key defense molecules originally identified in Drosophila, Toll-like receptor (TLR) superfamily members play a fundamental role in detecting invading pathogens or damage and initiating the innate immune system of mammalian cells. The skin, the largest organ of the human body, protects the human body by providing a critical physical and immunological active multilayered barrier against invading pathogens and environmental factors. At the first line of defense, the skin is constantly exposed to pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), and TLRs, expressed in a cell type-specific manner by various skin cells, serve as key molecules to recognize PAMPs and DAMPs and to initiate downstream innate immune host responses. While TLR-initiated inflammatory responses are necessary for pathogen clearance and tissue repair, aberrant activation of TLRs will exaggerate T cell-mediated autoimmune activation, leading to unwanted inflammation, and the development of several skin diseases, including psoriasis, atopic dermatitis, systemic lupus erythematosus, diabetic foot ulcers, fibrotic skin diseases, and skin cancers. Together, TLRs are at the interface between innate immunity and adaptive immunity. In this review, we will describe current understanding of the role of TLRs in skin defense and in the pathogenesis of psoriasis and atopic dermatitis, and we will also discuss the development and therapeutic effect of TLR-targeted therapies.
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27

Harrison, Rene E., and Sergio Grinstein. "Phagocytosis and the microtubule cytoskeleton." Biochemistry and Cell Biology 80, no. 5 (October 1, 2002): 509–15. http://dx.doi.org/10.1139/o02-142.

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Phagocytosis is a critical host defense mechanism used by macrophages and neutrophils to clear invading pathogens. The complex sequence of events resulting in internalization and degradation of the pathogens is a coordinated process involving lipids, signaling proteins, and the cytoskeleton. Here, we examine the role of the microtubule cytoskeleton in supporting both the engulfment of pathogens and their elimination within phagolysosomes.Key words: macrophage, microtubule, phagocytosis, maturation, Fc receptor.
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28

Heller, Kira. "Dana Philpott: Exploring the land of NOD." Journal of Experimental Medicine 206, no. 4 (April 13, 2009): 728–29. http://dx.doi.org/10.1084/jem.2064pi.

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29

Li, Yao, Shou-Long Deng, Zheng-Xing Lian, and Kun Yu. "Roles of Toll-Like Receptors in Nitroxidative Stress in Mammals." Cells 8, no. 6 (June 12, 2019): 576. http://dx.doi.org/10.3390/cells8060576.

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Free radicals are important antimicrobial effectors that cause damage to DNA, membrane lipids, and proteins. Professional phagocytes produce reactive oxygen species (ROS) and reactive nitrogen species (RNS) that contribute towards the destruction of pathogens. Toll-like receptors (TLRs) play a fundamental role in the innate immune response and respond to conserved microbial products and endogenous molecules resulting from cellular damage to elicit an effective defense against invading pathogens, tissue injury, or cancer. In recent years, several studies have focused on how the TLR-mediated activation of innate immune cells leads to the production of pro-inflammatory factors upon pathogen invasion. Here, we review recent findings that indicate that TLRs trigger a signaling cascade that induces the production of reactive oxygen and nitrogen species.
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30

Kuhn, Christoph. "Immune Response to a Variable Pathogen: A Stochastic Model with Two Interlocked Darwinian Entities." Computational and Mathematical Methods in Medicine 2012 (2012): 1–17. http://dx.doi.org/10.1155/2012/784512.

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This paper presents the modeling of a host immune system, more precisely the immune effector cell and immune memory cell population, and its interaction with an invading pathogen population. It will tackle two issues of interest; on the one hand, in defining a stochastic model accounting for the inherent nature of organisms in population dynamics, namely multiplication with mutation and selection; on the other hand, in providing a description of pathogens that may vary their antigens through mutations during infection of the host. Unlike most of the literature, which models the dynamics with first-order differential equations, this paper proposes a Galton-Watson type branching process to describe stochastically by whole distributions the population dynamics of pathogens and immune cells. In the first model case, the pathogen of a given type is either eradicated or shows oscillatory chronic response. In the second model case, the pathogen shows variational behavior changing its antigen resulting in a prolonged immune reaction.
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31

Kounatidis, Ilias, and Petros Ligoxygakis. "Drosophila as a model system to unravel the layers of innate immunity to infection." Open Biology 2, no. 5 (May 2012): 120075. http://dx.doi.org/10.1098/rsob.120075.

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Summary Innate immunity relies entirely upon germ-line encoded receptors, signalling components and effector molecules for the recognition and elimination of invading pathogens. The fruit fly Drosophila melanogaster with its powerful collection of genetic and genomic tools has been the model of choice to develop ideas about innate immunity and host–pathogen interactions. Here, we review current research in the field, encompassing all layers of defence from the role of the microbiota to systemic immune activation, and attempt to speculate on future directions and open questions.
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32

Suttorp, Norbert, and Stefan Hippenstiel. "Interaction of pathogens with the endothelium." Thrombosis and Haemostasis 89, no. 01 (2003): 18–24. http://dx.doi.org/10.1055/s-0037-1613538.

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SummaryThe endothelium lines the inner surface of the vessel wall establishing a multifunctional, semi-permeable cellular barrier at blood-tissue interface. The large total surface of the endothelium is exposed to pathogens, pathogen-derived products as well as to agents of the activated host defense during an inflammatory reaction. The endothelium is not only specifically targeted by important infective agents like Rickettsiae (1) or Bartonella (2), it is involved in virtually most, if not all, acute inflammatory responses. Pathogens attack the endothelium by a wide variety of strategies, as different as activation of preformed receptor-mediated pathways in the endothelium, release of pore-forming exotoxins or intracellular replication and chronic parasitism. These pathophysiological forces affect the endothelial phenotype, resulting in endothelial barrier dysfunction, increased leukocyte-endothelial interaction, mediator release, and procoagulant activity. Moreover, endothelial responses retroact on the invading pathogen as well as on the host defense resulting in a complex and dynamic interaction (Fig. 1). Endothelial activation contributes considerably to inflammation and resulting clinical characteristics. In this context the endothelium is not just a passive victim, it rather aggravates the ongoing struggle with the pathogen. In this review we focus on some important mechanisms of the cellular microbiology of endothelial infection by bacteria and viruses.
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33

Parnell, S., T. R. Gottwald, C. A. Gilligan, N. J. Cunniffe, and F. van den Bosch. "The Effect of Landscape Pattern on the Optimal Eradication Zone of an Invading Epidemic." Phytopathology® 100, no. 7 (July 2010): 638–44. http://dx.doi.org/10.1094/phyto-100-7-0638.

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A number of high profile eradication attempts on plant pathogens have recently been attempted in response to the increasing number of introductions of economically significant nonnative pathogen species. Eradication programs involve the removal of a large proportion of a host population and can thus lead to significant social and economic costs. In this paper we use a spatially explicit stochastic model to simulate an invading pathogen and show that it is possible to identify an optimal control radius, i.e., one that minimizes the total number of hosts removed during an eradication campaign that is effective in eradicating the pathogen. However, by simulating the epidemic and eradication processes in multiple landscapes, we demonstrate that the optimal radius depends critically on landscape pattern (i.e., the spatial configuration of hosts within the landscape). In particular, we find that the optimal radius, and also the number of host removals associated with it, increases with both the level of aggregation and the density of hosts in the landscape. The result is of practical significance and demonstrates that the location of an invading epidemic should be a key consideration in the design of future eradication strategies.
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34

Medina, Eva, and Dominik Hartl. "Myeloid-Derived Suppressor Cells in Infection: A General Overview." Journal of Innate Immunity 10, no. 5-6 (2018): 407–13. http://dx.doi.org/10.1159/000489830.

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After initial infection, the immune response that serves to restrict the invading pathogen needs to be tightly calibrated in order to avoid collateral immunopathological damage. This calibration is performed by specialized suppressor mechanisms, which are capable of dampening overwhelming or unremitting inflammation in order to prevent tissue damage. Myeloid-derived suppressor cells (MDSC) are emerging as key players in counter-balancing inflammatory responses and pathogenesis during infection. However, some pathogens are able to exploit the suppressive activities of MDSC to favor pathogen persistence and chronic infections. In this article, we review the current knowledge about the importance of MDSC in the context of bacterial, virus, parasites, and fungal infections.
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35

Kerrigan, Steve W., and Alastair Poole. "Focusing on the role of platelets in immune defence against invading pathogens." Platelets 26, no. 4 (April 24, 2015): 285. http://dx.doi.org/10.3109/09537104.2015.1038230.

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Fujita, Naonobu, Eiji Morita, Takashi Itoh, Atsushi Tanaka, Megumi Nakaoka, Yuki Osada, Tetsuo Umemoto, et al. "Recruitment of the autophagic machinery to endosomes during infection is mediated by ubiquitin." Journal of Cell Biology 203, no. 1 (October 7, 2013): 115–28. http://dx.doi.org/10.1083/jcb.201304188.

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Although ubiquitin is thought to be important for the autophagic sequestration of invading bacteria (also called xenophagy), its precise role remains largely enigmatic. Here we determined how ubiquitin is involved in this process. After invasion, ubiquitin is conjugated to host cellular proteins in endosomes that contain Salmonella or transfection reagent–coated latex (polystyrene) beads, which mimic invading bacteria. Ubiquitin is recognized by the autophagic machinery independently of the LC3–ubiquitin interaction through adaptor proteins, including a direct interaction between ubiquitin and Atg16L1. To ensure that invading pathogens are captured and degraded, Atg16L1 targeting is secured by two backup systems that anchor Atg16L1 to ubiquitin-decorated endosomes. Thus, we reveal that ubiquitin is a pivotal molecule that connects bacteria-containing endosomes with the autophagic machinery upstream of LC3.
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Künstler, András, Gábor Gullner, Attila L. Ádám, Judit Kolozsváriné Kolozsváriné Nagy, and Lóránt Király. "The Versatile Roles of Sulfur-Containing Biomolecules in Plant Defense—A Road to Disease Resistance." Plants 9, no. 12 (December 3, 2020): 1705. http://dx.doi.org/10.3390/plants9121705.

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Sulfur (S) is an essential plant macronutrient and the pivotal role of sulfur compounds in plant disease resistance has become obvious in recent decades. This review attempts to recapitulate results on the various functions of sulfur-containing defense compounds (SDCs) in plant defense responses to pathogens. These compounds include sulfur containing amino acids such as cysteine and methionine, the tripeptide glutathione, thionins and defensins, glucosinolates and phytoalexins and, last but not least, reactive sulfur species and hydrogen sulfide. SDCs play versatile roles both in pathogen perception and initiating signal transduction pathways that are interconnected with various defense processes regulated by plant hormones (salicylic acid, jasmonic acid and ethylene) and reactive oxygen species (ROS). Importantly, ROS-mediated reversible oxidation of cysteine residues on plant proteins have profound effects on protein functions like signal transduction of plant defense responses during pathogen infections. Indeed, the multifaceted plant defense responses initiated by SDCs should provide novel tools for plant breeding to endow crops with efficient defense responses to invading pathogens.
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Fingerhut, Leonie, Gaby Dolz, and Nicole de Buhr. "What Is the Evolutionary Fingerprint in Neutrophil Granulocytes?" International Journal of Molecular Sciences 21, no. 12 (June 25, 2020): 4523. http://dx.doi.org/10.3390/ijms21124523.

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Over the years of evolution, thousands of different animal species have evolved. All these species require an immune system to defend themselves against invading pathogens. Nevertheless, the immune systems of different species are obviously counteracting against the same pathogen with different efficiency. Therefore, the question arises if the process that was leading to the clades of vertebrates in the animal kingdom—namely mammals, birds, amphibians, reptiles, and fish—was also leading to different functions of immune cells. One cell type of the innate immune system that is transmigrating as first line of defense in infected tissue and counteracts against pathogens is the neutrophil granulocyte. During the host–pathogen interaction they can undergo phagocytosis, apoptosis, degranulation, and form neutrophil extracellular traps (NETs). In this review, we summarize a wide spectrum of information about neutrophils in humans and animals, with a focus on vertebrates. Special attention is kept on the development, morphology, composition, and functions of these cells, but also on dysfunctions and options for cell culture or storage.
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39

Thatcher, Louise F., Jonathan P. Anderson, and Karam B. Singh. "Plant defence responses: what have we learnt from Arabidopsis?" Functional Plant Biology 32, no. 1 (2005): 1. http://dx.doi.org/10.1071/fp04135.

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To overcome the attack of invading pathogens, a plant’s defence system relies on preformed and induced responses. The induced responses are activated following detection of a pathogen, with the subsequent transmission of signals and orchestrated cellular events aimed at eliminating the pathogen and preventing its spread. Numerous studies are proving that the activated signalling pathways are not simply linear, but rather, form complex networks where considerable cross talk takes place. This review covers the recent application of powerful genetic and genomic approaches to identify key defence signalling pathways in the model plant Arabidopsis thaliana (L.) Heynh. The identification of key regulatory components of these pathways may offer new approaches to increase the defence capabilities of crop plants.
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Mok, Adley CH, Christopher H. Mody, and Shu Shun Li. "Immune Cell Degranulation in Fungal Host Defence." Journal of Fungi 7, no. 6 (June 16, 2021): 484. http://dx.doi.org/10.3390/jof7060484.

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Humans have developed complex immune systems that defend against invading microbes, including fungal pathogens. Many highly specialized cells of the immune system share the ability to store antimicrobial compounds in membrane bound organelles that can be immediately deployed to eradicate or inhibit growth of invading pathogens. These membrane-bound organelles consist of secretory vesicles or granules, which move to the surface of the cell, where they fuse with the plasma membrane to release their contents in the process of degranulation. Lymphocytes, macrophages, neutrophils, mast cells, eosinophils, and basophils all degranulate in fungal host defence. While anti-microbial secretory vesicles are shared among different immune cell types, information about each cell type has emerged independently leading to an uncoordinated and confusing classification of granules and incomplete description of the mechanism by which they are deployed. While there are important differences, there are many similarities in granule morphology, granule content, stimulus for degranulation, granule trafficking, and release of granules against fungal pathogens. In this review, we describe the similarities and differences in an attempt to translate knowledge from one immune cell to another that may facilitate further studies in the context of fungal host defence.
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Hussain, Abid, Muhammad Waqar Ali, Ahmed Mohammed AlJabr, and Saad Naser AL-Kahtani. "Insights into the Gryllus bimaculatus Immune-Related Transcriptomic Profiling to Combat Naturally Invading Pathogens." Journal of Fungi 6, no. 4 (October 18, 2020): 232. http://dx.doi.org/10.3390/jof6040232.

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Natural pathogen pressure is an important factor that shapes the host immune defense mechanism. The current study primarily aimed to explore the molecular basis of the natural immune defense mechanism of a sporadic pest, Gryllus bimaculatus, during swarming by constructing cDNA libraries of the female mid-gut, male mid-gut, testes, and ovaries. The Illumina HiSeq platform generated an average of 7.9 G, 11.77 G, 10.07 G, and 10.07 G bases of outputs from the male mid-gut, female mid-gut, testes, and ovaries and libraries, respectively. The transcriptome of two-spotted field crickets was assembled into 233,172 UniGenes, which yielded approximately 163.58 million reads. On the other hand, there were 43,055 genes in common that were shared among all the biological samples. Gene Ontology analysis successfully annotated 492 immune-related genes, which comprised mainly Pattern Recognition Receptors (62 genes), Signal modulators (57 genes), Signal transduction (214 genes), Effectors (36 genes), and another immune-related 123 genes. In summary, the identified wide range of immune-related genes from G. bimaculatus indicates the existence of a sophisticated and specialized broad spectrum immune mechanism against invading pathogens, which provides, for the first time, insights into the molecular mechanism of disease resistance among two-spotted field crickets.
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42

Lea, S. "Interactions of CD55 with non-complement ligands." Biochemical Society Transactions 30, no. 6 (November 1, 2002): 1014–19. http://dx.doi.org/10.1042/bst0301014.

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Decay Accelerating Factor (or CD55) is a major regulator of the alternative and classical pathways of complement activation and is expressed on all serum-exposed cells. It is commonly hijacked by invading pathogens, including many enteroviruses and uropathogenic Escherichia coli, to promote cellular attachment prior to infection. This review will attempt to summarize our knowledge about these interactions between CD55 and various pathogens and also what is known about the non-complement interaction between CD55 and CD97.
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Mauthe, Mario, Wenqi Yu, Oleg Krut, Martin Krönke, Friedrich Götz, Horst Robenek, and Tassula Proikas-Cezanne. "WIPI-1 Positive Autophagosome-Like Vesicles Entrap PathogenicStaphylococcus aureusfor Lysosomal Degradation." International Journal of Cell Biology 2012 (2012): 1–13. http://dx.doi.org/10.1155/2012/179207.

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Invading pathogens provoke the autophagic machinery and, in a process termed xenophagy, the host cell survives because autophagy is employed as a safeguard for pathogens that escaped phagosomes. However, some pathogens can manipulate the autophagic pathway and replicate within the niche of generated autophagosome-like vesicles. By automated fluorescence-based high content analyses, we demonstrate thatStaphylococcus aureusstrains (USA300, HG001, SA113) stimulate autophagy and become entrapped in intracellular PtdIns(3)P-enriched vesicles that are decorated with human WIPI-1, an essential PtdIns(3)P effector of canonical autophagy and membrane protein of both phagophores and autophagosomes. Further,agr-positiveS. aureus(USA300, HG001) strains were more efficiently entrapped in WIPI-1 positive autophagosome-like vesicles when compared toagr-negative cells (SA113). By confocal and electron microscopy we provide evidence that single- and multiple-Staphylococci entrapped undergo cell division. Moreover, the number of WIPI-1 positive autophagosome-like vesicles entrapping Staphylococci significantly increased upon (i) lysosomal inhibition by bafilomycin A1and (ii) blocking PIKfyve-mediated PtdIns(3,5)P2generation by YM201636. In summary, our results provide evidence that the PtdIns(3)P effector function of WIPI-1 is utilized during xenophagy ofStaphylococcus aureus. We suggest that invadingS. aureuscells become entrapped in autophagosome-like WIPI-1 positive vesicles targeted for lysosomal degradation in nonprofessional host cells.
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Eisele, Nicholas A., and Deborah M. Anderson. "Host Defense and the Airway Epithelium: Frontline Responses That Protect against Bacterial Invasion and Pneumonia." Journal of Pathogens 2011 (2011): 1–16. http://dx.doi.org/10.4061/2011/249802.

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Airway epithelial cells are the first line of defense against invading microbes, and they protect themselves through the production of carbohydrate and protein matrices concentrated with antimicrobial products. In addition, they act as sentinels, expressing pattern recognition receptors that become activated upon sensing bacterial products and stimulate downstream recruitment and activation of immune cells which clear invading microbes. Bacterial pathogens that successfully colonize the lungs must resist these mechanisms or inhibit their production, penetrate the epithelial barrier, and be prepared to resist a barrage of inflammation. Despite the enormous task at hand, relatively few virulence factors coordinate the battle with the epithelium while simultaneously providing resistance to inflammatory cells and causing injury to the lung. Here we review mechanisms whereby airway epithelial cells recognize pathogens and activate a program of antibacterial pathways to prevent colonization of the lung, along with a few examples of how bacteria disrupt these responses to cause pneumonia.
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Behl, Jyotsna Dhingra, N. K. Verma, Neha Tyagi, Priyanka Mishra, Rahul Behl, and B. K. Joshi. "The Major Histocompatibility Complex in Bovines: A Review." ISRN Veterinary Science 2012 (May 28, 2012): 1–12. http://dx.doi.org/10.5402/2012/872710.

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Productivity in dairy cattle and buffaloes depends on the genetic factors governing the production of milk and milk constituents as well as genetic factors controlling disease resistance or susceptibility. The immune system is the adaptive defense system that has evolved in vertebrates to protect them from invading pathogens and also carcinomas. It is remarkable in the sense that it is able to generate an enormous variety of cells and biomolecules which interact with each other in numerous ways to form a complex network that helps to recognize, counteract, and eliminate the apparently limitless number of foreign invading pathogens/molecules. The major histocompatibility complex which is found to occur in all mammalian species plays a central role in the development of the immune system. It is an important candidate gene involved in susceptibility/resistance to various diseases. It is associated with intercellular recognition and with self/nonself discrimination. It plays major role in determining whether transplanted tissue will be accepted as self or rejected as foreign.
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46

Liaskou, Evaggelia, Daisy V. Wilson, and Ye H. Oo. "Innate Immune Cells in Liver Inflammation." Mediators of Inflammation 2012 (2012): 1–21. http://dx.doi.org/10.1155/2012/949157.

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Innate immune system is the first line of defence against invading pathogens that is critical for the overall survival of the host. Human liver is characterised by a dual blood supply, with 80% of blood entering through the portal vein carrying nutrients and bacterial endotoxin from the gastrointestinal tract. The liver is thus constantly exposed to antigenic loads. Therefore, pathogenic microorganism must be efficiently eliminated whilst harmless antigens derived from the gastrointestinal tract need to be tolerized in the liver. In order to achieve this, the liver innate immune system is equipped with multiple cellular components; monocytes, macrophages, granulocytes, natural killer cells, and dendritic cells which coordinate to exert tolerogenic environment at the same time detect, respond, and eliminate invading pathogens, infected or transformed self to mount immunity. This paper will discuss the innate immune cells that take part in human liver inflammation, and their roles in both resolution of inflammation and tissue repair.
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47

Ekanayake, Gayani, Erica D. LaMontagne, and Antje Heese. "Never Walk Alone: Clathrin-Coated Vesicle (CCV) Components in Plant Immunity." Annual Review of Phytopathology 57, no. 1 (August 25, 2019): 387–409. http://dx.doi.org/10.1146/annurev-phyto-080417-045841.

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At the host–pathogen interface, the protein composition of the plasma membrane (PM) has important implications for how a plant cell perceives and responds to invading microbial pathogens. A plant's ability to modulate its PM composition is critical for regulating the strength, duration, and integration of immune responses. One mechanism by which plant cells reprogram their cell surface is vesicular trafficking, including secretion and endocytosis. These trafficking processes add or remove cargo proteins (such as pattern-recognition receptors, transporters, and other proteins with immune functions) to or from the PM via small, membrane-bound vesicles. Clathrin-coated vesicles (CCVs) that form at the PM and trans-Golgi network/early endosomes have emerged as the prominent vesicle type in the regulation of plant immune responses. In this review, we discuss the roles of the CCV core, adaptors, and accessory components in plant defense signaling and immunity against various microbial pathogens.
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48

Thompson, Robin N., Richard C. Cobb, Christopher A. Gilligan, and Nik J. Cunniffe. "Management of invading pathogens should be informed by epidemiology rather than administrative boundaries." Ecological Modelling 324 (March 2016): 28–32. http://dx.doi.org/10.1016/j.ecolmodel.2015.12.014.

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49

Morey, Jacqueline R., Christopher A. McDevitt, and Thomas E. Kehl-Fie. "Host-imposed manganese starvation of invading pathogens: two routes to the same destination." BioMetals 28, no. 3 (April 3, 2015): 509–19. http://dx.doi.org/10.1007/s10534-015-9850-z.

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50

Zhang, Ji, and Serge Rivest. "Is Survival Possible Without Arachidonate Metabolites in the Brain During Systemic Infection?" Physiology 18, no. 4 (August 2003): 137–42. http://dx.doi.org/10.1152/nips.01415.2002.

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The central nervous system mediates a coordinated set of biological responses during systemic immune stimuli. These responses are essential for the organism to eliminate invading pathogens and restore health. Coincidentally, centrally produced prostaglandins play a determinant role in activating the neuronal circuits involved in the control of autonomic functions.
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