[PP.18.01] DECREASED CIRCULATING T REGULATORY LYMPHOCYTES IN OBESE PATIENTS UNDERGOING BARIATRIC SURGERY
Claudia Agabiti RoseiClaudia RossiniFrancesco MittempergherAmin TitiNazario PortolaniCarolina De CiuceisStefano CalettiMaria Antonietta CoschignanoValentina TraplettiE. PorteriP. PileriEnrico Agabiti RoseiDamiano Rizzoni
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Objective: It has been previously demonstrated that T lymphocytes may be involved in the development of hypertension and microvascular remodeling, and that circulating T effector lymphocytes may be increased in hypertension (De Ciuceis C et al, Am J Hypertens 2016 Sep 21 online printing; Itani HA et al. Hypertension 2016; 68:123–132). In particular, Th1 and Th 17 lymphocytes may contribute to the progression of hypertension and microvascular damage while TREG lymphocytes seem to be protective. However, no data is avaliable about patients with severe obesity, in which pronounced microvascular alterations were observed (De Ciuceis C et al, Hypertension 2011; 58:29–36). Design and method: We have investigated 32 severely obese patients undergoing bariatric surgery, as well as 24 normotensive lean subjects and 11 hypertensive lean subjects undergoing an election surgical intervention. No sign of local or systemic inflammation was present in any subject or patient. A peripheral blood sample was obtained before surgery for assessment of CD4+ T lymphocyte subpopulations. Lymphocyte phenotype was evaluated by flow cytometry in order to assess T-effector and T-regulatory (TREG) lymphocytes. Subsets of TREGS were defined as follows: -TREGS recent thymic emigrants (RTE), directly derived from thymus: CD31+; -TREGS naïve: CCR7+CD45RA+; -TREGS central memory (CM): CCR7+CD45RA-; -TREGS effector memory (EM): CCR7-CD45RA-; -TREGS terminal differentiated effector memory (TDEM): CCR7-CD45RA+. Results: Results are summarized in the Table (*p < 0.05, **p < 0.01, ***p < 0.001 vs. lean normotensives; #p < 0.05, ##p < 0.01, ###p < 0.001 vs. lean hypertensives). A marked reduction of several TREG subpopolations was observed in obese patients compared with controls, together with an increased in some T-effector cells.Conclusions: TREG lymphocytes are clearly reduced in severely obese patients, possibly contributing to the development of marked microvascular alterations previously observed in such a population.Cite
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Horticultural crops suffer from bacterial, fungal, and oomycete pathogens. Effectors are one of the main weapons deployed by those pathogens, especially in the early stages of infection. Pathogens secrete effectors with diverse functions to avoid recognition by plants, inhibit or manipulate plant immunity, and induce programmed cell death. Most identified effectors are proteinaceous, such as the well-studied type-III secretion system effectors (T3SEs) in bacteria, RXLR and CRN (crinkling and necrosis) motif effectors in oomycetes, and LysM (lysin motifs) domain effectors in fungi. In addition, some non-proteinaceous effectors such as toxins and sRNA also play crucial roles in infection. To cope with effectors, plants have evolved specific mechanisms to recognize them and activate effector-triggered immunity (ETI). This review summarizes the functions and mechanisms of action of typical proteinaceous and non-proteinaceous effectors secreted by important horticultural crop pathogens. The defense responses of plant hosts are also briefly introduced. Moreover, potential application of effector biology in disease management and the breeding of resistant varieties is discussed.
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Plant Immunity
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There is a continuous arms race between pathogens and their host plants. However, successful pathogens, such as phytopathogenic oomycetes, secrete effector proteins to manipulate host defense responses for disease development. Structural analyses of these effector proteins reveal the existence of regions that fail to fold into three-dimensional structures, intrinsically disordered regions (IDRs). Because of their flexibility, these regions are involved in important biological functions of effector proteins, such as effector-host protein interactions that perturb host immune responses. Despite their significance, the role of IDRs in phytopathogenic oomycete effector-host protein interactions is not clear. This review, therefore, searched the literature for functionally characterized oomycete intracellular effectors with known host interactors. We further classify regions that mediate effector-host protein interactions into globular or disordered binding sites in these proteins. To fully appreciate the potential role of IDRs, five effector proteins encoding potential disordered binding sites were used as case studies. We also propose a pipeline that can be used to identify, classify as well as characterize potential binding regions in effector proteins. Understanding the role of IDRs in these effector proteins can aid in the development of new disease-control strategies.
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The ability to secrete effector proteins that can enter plant cells and manipulate host processes is a key determinant of what makes a successful plant pathogen. Here, we review intracellular effectors from filamentous (fungal and oomycete) phytopathogens and the host proteins and processes that are targeted to promote disease. We cover contrasting virulence strategies and effector modes of action. Filamentous pathogen effectors alter the fates of host proteins that they target, changing their stability, their activity, their location, and the protein partners with which they interact. Some effectors inhibit target activity, whereas others enhance or utilize it, and some target multiple host proteins. We discuss the emerging topic of effectors that target negative regulators of immunity or other plant proteins with activities that support susceptibility. We also highlight the commonly targeted host proteins that are manipulated by effectors from multiple pathogens, including those representing different kingdoms of life.
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Abstract Microbial plant pathogens use secreted effector proteins for successful infection of their host. This evolved state is rather exceptional as most microbes do not cause disease in the vast majority of plant species. An important primary activity of effectors is to interfere with a range of plant immune processes to evade and suppress pathogen detection, or to block immune signalling and downstream responses. Furthermore, effectors can enhance disease susceptibility by altering cellular processes and modulating host transcription. For most of these activities, effectors specifically target plant proteins that are central in these processes. An advanced virulence strategy is the post‐translational modification by effectors of plant targets to change their activity or stability. The knowledge gathered on the molecular mechanisms underlying effector‐triggered susceptibility of plants provides great potential for novel approaches of resistance breeding. Key Concepts Pathogens secrete and/or translocate effector proteins to promote plant disease. Besides their primary role in promoting disease, effectors or effector‐modified plant proteins can be recognised by resistance proteins to activate an effector‐triggered immune response. Many effectors block pathogen‐associated molecular pattern (PAMP)‐triggered immunity and/or effector‐triggered immunity. Other effectors rewire signalling pathways and reprogramme the plant cell to promote pathogen growth. Certain effectors can affect the activity or function of host proteins by post‐translational modifications e.g. (de)phosphorylation or targeting for proteosomal degradation.
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Plants can be colonized by fungi that have adopted highly diverse lifestyles, ranging from symbiotic to necrotrophic. Colonization is governed in all systems by hundreds of secreted fungal effector molecules. These effectors suppress plant defense responses and modulate plant physiology to accommodate fungal invaders and provide them with nutrients. Fungal effectors either function in the interaction zone between the fungal hyphae and host or are transferred to plant cells. This review describes the effector repertoires of 84 plant-colonizing fungi. We focus on the mechanisms that allow these fungal effectors to promote virulence or compatibility, discuss common plant nodes that are targeted by effectors, and provide recent insights into effector evolution. In addition, we address the issue of effector uptake in plant cells and highlight open questions and future challenges.
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Plant diseases caused by fungal pathogens are typically initiated by molecular interactions between ‘effector’ molecules released by a pathogen and receptor molecules on or within the plant host cell. In many cases these effector-receptor interactions directly determine host resistance or susceptibility. The search for fungal effector proteins is a developing area in fungal-plant pathology, with more than 165 distinct confirmed fungal effector proteins in the public domain. For a small number of these, novel effectors can be rapidly discovered across multiple fungal species through the identification of known effector homologues. However, many have no detectable homology by standard sequence-based search methods. This study employs a novel comparison method (RemEff) that is capable of identifying protein families with greater sensitivity than traditional homology-inference methods, leveraging a growing pool of confirmed fungal effector data to enable the prediction of novel fungal effector candidates by protein family association. Resources relating to the RemEff method and data used in this study are available from https://figshare.com/projects/Effector_protein_remote_homology/87965 .
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Effectors are small, secreted molecules that mediate the establishment of interactions in nature. While some concepts of effector biology have stood the test of time, this area of study is ever-evolving as new effectors and associated characteristics are being revealed. In the present review, the different characteristics that underly effector classifications are discussed, contrasting past and present knowledge regarding these molecules to foster a more comprehensive understanding of effectors for the reader. Research gaps in effector identification and perspectives for effector application in plant disease management are also presented, with a focus on fungal effectors in the plant-microbe interaction and interactions beyond the plant host. In summary, the review provides an amenable yet thorough introduction to fungal effector biology, presenting noteworthy examples of effectors and effector studies that have shaped our present understanding of the field.
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