Relevant bibliographies by topics / Immuno evasione

Academic literature on the topic 'Immuno evasione'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Immuno evasione"

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Baldwin, Louise A., Nenad Bartonicek, Jessica Yang, Sunny Z. Wu, Niantao Deng, Daniel Roden, Chia-Ling Chan, et al. "Abstract P1-04-04: Dna barcoding reveals ongoing immunoediting of clonal cancer populations during metastatic progression and in response to immunotherapy." Cancer Research 82, no. 4_Supplement (February 15, 2022): P1–04–04—P1–04–04. http://dx.doi.org/10.1158/1538-7445.sabcs21-p1-04-04.

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Abstract As cancers develop and spread they must continually evade immune destruction. Understanding mechanisms of immune evasion in cancer is clinically significant as demonstrated with the successes of immune checkpoint inhibitors. Breast cancer is known to be highly immune evasive and responds poorly to the current immunotherapies, indicating alternative immune pathways must be targeted. We hypothesise that there are unidentified genetic mechanisms that enable immune evasion in breast cancer. We aim to uncover and target these mechanisms to sensitise immune evasive breast cancer cells to immune destruction in the context of immunotherapy treatment. DNA barcoding technology offers a new approach to understanding immune evasion. By stably integrating a unique DNA barcode sequence into each cell, we can study clonal immune evasion in vivo. Using this technology, we identified cancer cell clones from the 4T1 murine mammary carcinoma cell line that are highly enriched in lung metastases following treatment with combination immunotherapy (anti-CTLA-4 plus anti-PD-1). We isolated these specific immune evasive clones and established them as clonal cell lines. We have identified stark clonal differences in both PD-L1 and MHC I expression at both the RNA and protein level, and shown that MHC I expression is only partially controlled by epigenetic mechanisms. In addition, immune evasive subclones co-cultured with stimulated T cells resulted in less activated T cells than their less evasive counterparts. Furthermore, RNA sequencing of these clones has identified a gene signature that is strongly associated with decreased survival in both the METABRIC and TCGA cohorts. We have demonstrated ongoing immunoediting in the 4T1 model in vivo, both during metastasis and immunotherapy treatment. We have also identified subclonal populations of cells within a single tumour utilising different mechanisms of immune evasion. RNA sequencing has revealed a gene signature strongly associated with poor survival of basal-like breast cancer in two cohorts. Further pathway-level analysis of the resulting gene signature is required to elucidate the drivers of this aggressive and immune evasive phenotype. By targeting newly identified mechanisms of immune evasion in combination with current immunotherapies, we hope to improve the long-term survival of breast cancer patients. Citation Format: Louise A Baldwin, Nenad Bartonicek, Jessica Yang, Sunny Z Wu, Niantao Deng, Daniel Roden, Chia-Ling Chan, Ghamdan Al-Eryani, Damien J Zanker, Belinda S Parker, Alexander Swarbrick, Simon Junankar. Dna barcoding reveals ongoing immunoediting of clonal cancer populations during metastatic progression and in response to immunotherapy [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P1-04-04.
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Lehnert, Teresa, Maria T. E. Prauße, Kerstin Hünniger, Jan-Philipp Praetorius, Oliver Kurzai, and Marc Thilo Figge. "Comparative assessment of immune evasion mechanisms in human whole-blood infection assays by a systems biology approach." PLOS ONE 16, no. 4 (April 1, 2021): e0249372. http://dx.doi.org/10.1371/journal.pone.0249372.

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Computer simulations of mathematical models open up the possibility of assessing hypotheses generated by experiments on pathogen immune evasion in human whole-blood infection assays. We apply an interdisciplinary systems biology approach in which virtual infection models implemented for the dissection of specific immune mechanisms are combined with experimental studies to validate or falsify the respective hypotheses. Focusing on the assessment of mechanisms that enable pathogens to evade the immune response in the early time course of a whole-blood infection, the least-square error (LSE) as a measure for the quantitative agreement between the theoretical and experimental kinetics is combined with the Akaike information criterion (AIC) as a measure for the model quality depending on its complexity. In particular, we compare mathematical models with three different types of pathogen immune evasion as well as all their combinations: (i) spontaneous immune evasion, (ii) evasion mediated by immune cells, and (iii) pre-existence of an immune-evasive pathogen subpopulation. For example, by testing theoretical predictions in subsequent imaging experiments, we demonstrate that the simple hypothesis of having a subpopulation of pre-existing immune-evasive pathogens can be ruled out. Furthermore, in this study we extend our previous whole-blood infection assays for the two fungal pathogens Candida albicans and C. glabrata by the bacterial pathogen Staphylococcus aureus and calibrated the model predictions to the time-resolved experimental data for each pathogen. Our quantitative assessment generally reveals that models with a lower number of parameters are not only scored with better AIC values, but also exhibit lower values for the LSE. Furthermore, we describe in detail model-specific and pathogen-specific patterns in the kinetics of cell populations that may be measured in future experiments to distinguish and pinpoint the underlying immune mechanisms.
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Zindl, C. L., and D. D. Chaplin. "Tumor Immune Evasion." Science 328, no. 5979 (May 6, 2010): 697–98. http://dx.doi.org/10.1126/science.1190310.

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Seton-Rogers, Sarah. "Driving immune evasion." Nature Reviews Cancer 18, no. 2 (January 25, 2018): 67. http://dx.doi.org/10.1038/nrc.2018.5.

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Mueller, K. L. "Immune Evasion Tactic." Science Signaling 4, no. 157 (January 25, 2011): ec27-ec27. http://dx.doi.org/10.1126/scisignal.4157ec27.

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Mascola, John R. "Engineering immune evasion." Nature 441, no. 7090 (May 2006): 161. http://dx.doi.org/10.1038/441161a.

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Fehervari, Zoltan. "Glioma immune evasion." Nature Immunology 18, no. 5 (May 2017): 487. http://dx.doi.org/10.1038/ni.3736.

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Fitzpatrick, David R., and Helle Bielefeldt-Ohmann. "Mechanisms of herpesvirus immuno-evasion." Microbial Pathogenesis 10, no. 4 (April 1991): 253–59. http://dx.doi.org/10.1016/0882-4010(91)90009-y.

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Upadhyay, Ranjan, Linda Hammerich, Paul Peng, Brian Brown, Miriam Merad, and Joshua Brody. "Lymphoma: Immune Evasion Strategies." Cancers 7, no. 2 (April 30, 2015): 736–62. http://dx.doi.org/10.3390/cancers7020736.

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Tsukerman, Pinchas, Jonatan Enk, and Ofer Mandelboim. "Metastamir-mediated immune evasion." OncoImmunology 2, no. 1 (January 2013): e22245. http://dx.doi.org/10.4161/onci.22245.

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Dissertations / Theses on the topic "Immuno evasione"

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GAMBACORTA, VALENTINA. "Novel Insights into the Immunobiology of Leukemia Relapse after Allogeneic Hematopoietic Cell Transplantation." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2020. http://hdl.handle.net/10281/259336.

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Il numero di pazienti affetti da leucemia mieloide acuta (LMA) trattati con trapianto di cellule ematopoietiche allogeniche (TCE-allo) è in costante aumento. L'efficacia terapeutica di questa procedura si basa principalmente sul trasferimento dal donatore al paziente di cellule immunitarie, in grado di riconoscere ed eliminare le cellule tumorali residue. Tuttavia, fino al 50% dei pazienti trapiantati con LMA va incontro a recidiva e la prognosi di questi pazienti rimane estremamente negativa. Pertanto, lo scopo del mio lavoro di tesi era quello di migliorare la comprensione attuale dell'immunobiologia della recidiva post-trapianto, studiando i) come le terapie e la leucemia stessa influenzano la ricostituzione immunitaria, ii) come perfezionare il rilevamento della ricomparsa della leucemia nella fase di malattia minima residua (MMR) e iii) come scoprire i meccanismi molecolari alla base dell’evasione della leucemia dal sistema immune. In particolare, presenterò per la prima volta i risultati di uno studio prospettico volto a valutare l'utilità clinica di monitorare il chimerismo specifico del paziente sul sangue periferico, anziché sul midollo osseo attualmente utilizzato, impiegando la PCR quantitativa (PCRq) per la diagnosi precoce delle recidive di leucemia dopo trapianto. In seguito, saranno presentati i risultati di due studi sulla dinamica della ricostituzione delle cellule NK e T dopo il TCE-allo. Entrambi gli studi mirano a comprendere i determinanti dell'insufficienza del sistema immunitario del donatore nel controllo della recidiva della malattia LMA con la possibilità di utilizzare le caratteristiche identificate come biomarcatori per prevedere la recidiva post-trapianto. Nelle ultime sezioni presenterò dati sia pubblicati che non pubblicati sui meccanismi biologici della recidiva della malattia post-trapianto, riferendo in che modo questa conoscenza possa essere facilmente tradotta in nuove opzioni terapeutiche per combattere la recidiva della malattia. In queste sezioni sono incluse due recensioni che ho scritto di recente, focalizzate, rispettivamente, sull'immunobiologia della recidiva post-trapianto e sulle attuali terapie epigenetiche all’avanguardia per la LMA e i loro effetti sul sistema immunitario.
The number of acute myeloid leukemia (AML) patients cured through allogeneic hematopoietic cell transplantation (allo-HCT) is constantly increasing. The therapeutic effectiveness of this procedure mainly relies on the transfer from the donor to the patient of immune cells, capable of recognizing and eliminating residual tumor cells. Still, up to 50% of transplanted AML patients will eventually relapse, and the prognosis of these patients remains extremely poor. Thus, aim of my thesis work was to improve current understanding on the immunobiology of post-transplantation relapse, by investigating i) how therapies and leukemia itself affect immune reconstitution, ii) how to refine detection of leukemia reappearance at the stage minimal residual disease (MRD), and iii) how to uncover the molecular mechanisms at the basis of leukemia immune evasion. In particular, I will first present the results of a prospective study aiming at evaluating the clinical utility of monitoring patient-specific chimerism on peripheral blood, instead of the currently used bone marrow specimens, employing quantitative PCR (qPCR) for the early detection of leukemia relapses after transplantation. Will next present the results of two studies on the dynamics of recovery of NK and T cells after allo-HCT. Both studies aim at understanding the determinants of donor immune system failure in controlling AML disease recurrence with the potential implications of using the identified features as biomarkers to predict post-transplantation relapse. In the last sections I will present both published and unpublished data on the biological mechanisms underlying post-transplantation disease relapse, reporting how this knowledge can be easily translated in novel therapeutic rationales to combat disease recurrence. Included in these sections are two recent reviews I authored, focused, respectively, on the immunobiology of post-transplantation relapse, and on current state-of-the art epigenetic therapies for AML and their effects on the immune system.
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Close, Helen Judith. "Immune evasion in glioma." Thesis, University of Leeds, 2016. http://etheses.whiterose.ac.uk/16103/.

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Glioblastoma multiforme (GBM) is the most common form of primary brain cancer and the current prognosis for patients is poor. New therapies are required that target the invasive cells that are characteristic of GBM. GBM is infiltrated by immune cells but, as with other cancers, immune evasion pathways minimise productive anti-tumour immunity. Natural killer (NK) cells are able to recognise and kill tumour cells and are being developed for the immunotherapy of other cancers. The aim of this work was to analyse the interaction between human NK cells and GBM cells in vivo and in vitro, as a prerequisite to future NK cell based immunotherapy of GBM. Analysis of the cell surface phenotype for GBM infiltrating NK and T cells revealed that the tumour microenvironment exerts localised immune evasion mechanisms which downregulate activation receptors and upregulate inhibitory receptors. The interaction of NK cells with patient-derived GBM stem cells, which are thought to be responsible for recurrent disease, was investigated in vitro. A high-throughput, multiplex flow cytometry-based screen of tumour cells revealed the expression of a number of cell surface molecules that regulate NK cell activation. Furthermore, GBM cells were more susceptible to NK cell lysis in vitro compared to a non-cancerous neural progenitor cell line, revealing specificity in the NK cell response. Furthermore, this screen identified potential mechanisms by which GBM might evade immune surveillance in vivo. Targeting these pathways and restoring functional immune surveillance provides a potential route for future immunotherapy of this disease. However, GBM patients often experience cerebral oedema and are treated with immunosuppressive corticosteroids, such as dexamethasone; this induces a similar immunosuppressed phenotype to that observed with the GBM infiltrating NK cells, and inhibits their lytic function. Gene expression profiling identified the transcription factor c-Myc as a key regulator of NK cell activation and as a hub for the immunosuppressive action of steroids and the immunosuppressive cytokine TGF-β. The demonstration that therapeutic steroids target the same pathway as TGF-β and induce immunosuppression has important implications for the use of steroids in patients undergoing immunotherapy.
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Odeberg, Jenny. "Human cytomegalovirus immune evasion strategies /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-126-8.

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Rosa, Gustavo Luis Teixeira Lopes. "Studies of MHV-68 immune evasion and immune control." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611892.

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Solis, Mayra. "Immune evasion mechanisms by HIV-1." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103531.

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Induction of the innate immune response by viral pathogens is characterized by a rapid production of Type I interferons (IFNβ/α). Recognition of viral components by Toll-like receptors (TLRs) or RIG-I-like receptors (RLRs), initiates multiple intracellular signalling cascades that culminate in the activation of the transcription factor NF-B and the interferon regulatory factors-3 and 7 (IRF-3 and IRF-7). As a consequence, these events lead to the production of immunoregulatory molecules, including Type I IFNs, pro-inflammatory cytokines and IFN-stimulated genes (ISGs), resulting in the inhibition of virus replication. Throughout evolution, viruses have developed strategies to subvert the innate immune response for their own benefit. Human immunodeficiency virus type-1 (HIV-1), the etiological agent of the acquired immunodeficiency syndrome (AIDS), has been shown to evade the innate immune response, resulting in disease progression. Thus, understanding the distinct mechanisms by which HIV-1 modulates TLRs and RLRs signaling pathways will ultimately lead to the development of novel strategies to inhibit HIV-1 replication and propagation. Studies have indicated that TLRs that signal via NF-B enhance HIV-1 replication. However, TLR4 stimulation triggers both NF-B and the IFN pathway and thus may have inhibitory effects on HIV-1 replication. Our first study was aimed at better understanding the role of TLR4 in HIV-1 replication. Therefore, we first characterized IRF-3 and IRF-7 activation following TLR4 stimulation. Our results demonstrate that the non-canonical TBK1 and IKKε are activated with distinct kinetics resulting in the activation of IRF-3 and subsequent induction of Type I IFNs. Thus, activation of the IFN pathway via TLR4 stimulation can provide a novel strategy to inhibit HIV-1 replication. Our second study sought to further delineate the different signaling pathways activated by HIV-1. Accordingly, transcriptional changes induced by distinct HIV-1 subtypes in immature dendritic cells were examined by microarray analysis. Our findings demonstrate that during the late phase of HIV-1 infection, a subset of genes is differentially regulated by the subtypes. In addition, this study highlights the important role of immature dendritic cells in HIV-1 replication and dissemination. Finally, given the importance of RLRs in the recognition of RNA viruses, the objective of the final study was aimed at investigating the evasion mechanisms employed by HIV-1 to counteract the initial antiviral response. Our results reveal that HIV-1 RNA is detected by the cytosolic receptor RIG-I. However, the HIV-1 viral protease sequesters RIG-I to the lysosomes and thus inhibits RIG-I-mediated antiviral response. Overall, the research presented in this thesis provides new avenues for developing novel therapeutic and preventive strategies to combat HIV-1/AIDS.
L'induction de la réponse immunitaire innée par des pathogènes viraux est caractérisée par une production rapide des interférons de Type I (IFNβ/α). Les Toll-like (TLR) ou RIG-like (RLR) récepteurs détectent divers composants viraux induisant multiples voies de signalisation intracellulaire impliquées dans l'activation du factor de transcription-NF-B- ainsi que des facteurs de régulation de l'interféron-3 et -7 (IRF-3 et IRF-7). Ces évènements mènent à la synthèse de molécules immunorégulatrices, tel que les interférons (IFN) de Type I, les cytokines pro-inflammatoires et les gènes stimulés par l'IFN (ISG), qui jouent un rôle important dans l'inhibition de la réplication virale. Au cours de l'évolution, les virus ont développé des stratégies pour contrer la réponse immunitaire innée afin de se répliquer. Le virus de l'immunodéficience humaine de type 1(VIH-1), l'agent infectieux du syndrome de l'immunodéficience acquise (SIDA), échappe à la réponse immunitaire innée, ce qui favorise la progression de la maladie. Par conséquent, une meilleure compréhension des mécanismes par lesquels le VIH-1 module les voies de signalisation des TLR et des RLR pourrait mener au développement de nouvelles stratégies thérapeutiques pour empêcher la réplication et donc la propagation du VIH-1. Des études ont démontré que les TLR qui signalent par l'intermédiaire de NF-B augmentent la réplication du VIH-1. Cependant, la stimulation du TLR4 déclenche à la fois la voie de signalisation de NF-B et celle des IFN, pouvant avoir ainsi des effets inhibiteurs sur la réplication du VIH-1. L'objectif de notre première étude était de comprendre le rôle du TLR4 dans la réplication du VIH-1. Par conséquent, nous avons caractérisé la voie d'activation des IRF-3 et IRF-7 suite à la stimulation du TLR4. Nos résultats démontrent que les kinases non-canoniques TBK1et IKKε sont activées avec une cinétique distincte ayant pour conséquence l'activation de l'IRF-3 et l'induction subséquente des IFN de type I. Par conséquent, l'activation de la voie de signalisation des IFN par la stimulation du TLR4 pourrait offrir une nouvelle stratégie pour inhiber la réplication du VIH-1. Notre deuxième étude a eu pour but de définir les différentes voies de signalisation activées par le VIH-1. Les changements transcriptionels induits par les différents sous-types du VIH-1 dans les cellules dendritiques immatures ont été examinés par analyse de microréseaux. Nos résultats démontrent que pendant la phase tardive de l'infection VIH-1, un ensemble de gènes est différemment régulé par les différents sous-types du VIH-1. En plus, cette étude accentue le rôle important des cellules dendritiques immatures dans la réplication et la dissémination du VIH-1. En conclusion, étant donné l'importance des RLR dans la reconnaissance des virus à ARN, l'objectif de la dernière étude a été d'étudier les mécanismes d'évasion utilisés par VIH-1 pour contrer la réponse antivirale innée. Nos résultats démontrent que l'ARN du VIH-1 est détecté par le récepteur cytosolique RIG-I. Cependant, une protéine du VIH-1 -la protéase- séquestre le récepteur RIG-I dans les lysosomes et empêche l'activation de la réponse antivirale initié par le récepteur RIG-I. De façon générale, la recherche présentée dans cette thèse propose de nouvelles avenues pour développer des stratégies préventives et thérapeutiques afin de combattre le VIH-1/SIDA.
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Chan, Mei-po, and 陳美寶. "Modulation of Bacillus Calmétte Guerin-induced immune evasion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B40987607.

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Andrews, Sophie Marie. "Adaptive immune evasion in clinically latent HIV infection." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:b7416aab-d345-48df-9194-797c62d7db47.

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HIV is a master of immune evasion, utilising a range of different techniques to not only survive the human immune system, but also mediate its eventual catastrophic decline. Understanding how HIV evades the adaptive immune response is paramount to developing effective treatments and vaccines. This thesis aimed to investigate three key ways in which HIV-1 and HIV-2 mediate immune evasion in the context of clinically latent infection. Chapter three summarises a study into selection pressure and mutation in the gp120 envelope gene in a narrow-source HIV-1 cohort of former plasma donors (FPDs) from China. This study further characterised the cohort, and identified specific mutations in the gene consistent with antibody and CTL-driven selection pressure. Chapter four describes an investigation into the downregulation of HLA-I mediated by primary isolates of HIV-1 and HIV-2 Nef. Nef-mediated HLA-I downregulation contributes to the evasion of CTL responses. In stark contrast to previous reports, no evidence for differential downregulation of HLA-A and HLA-B was detected, but primary isolates invariably showed reduced activity relative to laboratory-adapted and consensus variants. In performing this study, a number of limitations came to light regarding how bifurcate analyses are used to interpret flow cytometric data collected in studies of receptor modulation. A novel technique - SWARM - was therefore developed to address these limitations, and is described in chapter five. Chapter six aimed to address why CTL responses against HIV-2 Nef are rare, despite HIV-1 Nef being highly immunogenic. A series of in vitro (immuno)proteasomal processing assays revealed HIV-2 Nef is more extensively digested than HIV-1 Nef, but further experimentation is required to explain the difference in response. Finally, chapter seven briefly summarises a successful collaborative attempt to resolve the first ever crystal structure of HIV-2 Nef.
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Ozturk, Mumin. "Tuberculosis transcriptomics: host protection and immune evasion mechanisms." Doctoral thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/26863.

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Mycobacterium tuberculosis (Mtb) is the leading cause of death from an infectious disease. The success of the pathogen lies in its ability to subvert hostile intracellular macrophage environment. We performed genome-wide transcriptional deep sequencing on total RNA in murine bone marrow-derived macrophages (BMDM) infected with hypervirulent Beijing strain (HN878) in an extensive time kinetic manner using single molecule sequencer and cap analysis gene expression (CAGE) technique. CAGE analysis revealed nearly 36000 unique RNA transcripts with approximately 16000 are not unannotated to a specific gene. This thesis addressed global changes in RNA expression levels in macrophages infected with Mtb in a time kinetic manner to pinpoint novel host protection and immune evasion genes and elucidate the role of these genes in vitro macrophage assays and in vivo knockout mouse studies. The data in this thesis showed that basic leucine zipper transcription factor 2 (Batf2) was an important factor that regulates inflammatory responses in Mtb infection. Deletion of Batf2 led to the survival of mice with reduced lung inflammation and histopathology due to reduced recruitment of inflammatory macrophages. We also showed that Batf2 was highly expressed in peripheral blood from adolescents who progressed from infection to tuberculosis disease and a predictive human biomarker for tuberculosis disease. In contrast to Batf2, we showed that Protein Kinase C-delta (PKC-δ) deficient mice are highly susceptible to tuberculosis and human lung proteomics dataset revealed that PKC-δ was highly upregulated in the necrotic and cavitory regions of human granulomas in multi-drug resistant subjects. PKC-δ deficient mice had a significant reduction in alveolar macrophages and dendritic cells, reduced accumulation of lipid bodies and serum fatty acids. In vitro experiments showed that PKCδ was required for optimal killing effector functions which were independent of phagosome maturation and autophagy in primary murine macrophages. Our studies suggested that these novel genes play a role in the immune response to Mtb and should be studied more thoroughly to evaluate their potential in possible TB interventions.
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Chan, Mei-po. "Modulation of Bacillus Calmétte Guerin-induced immune evasion." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B40987607.

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Akhtar, Lisa Nowoslawski. "The role of SOCS proteins in HIV immune evasion." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2010. https://www.mhsl.uab.edu/dt/2010p/akhtar.pdf.

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Books on the topic "Immuno evasione"

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PhD, Henderson Brian, and Oyston Petra C. F, eds. Bacterial evasion of host immune responses. Cambridge, UK: Cambridge University Press, 2003.

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Van der Ploeg, Lex H. T., Cantor Charles R. 1942-, and Vogel Henry J. 1920-, eds. Immune recognition and evasion: Molecular aspects of host-parasite interaction. San Diego: Academic Press, 1990.

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Su, Bin, Kai Deng, Christiane Moog, and R. Brad Jones, eds. Immune Evasion Mechanisms by RNA Viruses. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-903-4.

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Henderson, Brian, and Petra C. F. Oyston, eds. Bacterial Evasion of Host Immune Responses. Cambridge University Press, 2003. http://dx.doi.org/10.1017/cbo9780511546266.

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Henderson, Brian, and Petra C. F. Oyston. Bacterial Evasion of Host Immune Responses. Cambridge University Press, 2003.

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Henderson, Brian, and Petra C. F. Oyston. Bacterial Evasion of Host Immune Responses. Cambridge University Press, 2009.

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Henderson, Brian, and Petra C. F. Oyston. Bacterial Evasion of Host Immune Responses. Cambridge University Press, 2003.

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Henderson, Brian, and Petra C. F. Oyston. Bacterial Evasion of Host Immune Responses. Cambridge University Press, 2003.

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Wilson, Michael, Anthony Coates, Brian Henderson, and Petra C. F. Oyston. Bacterial Evasion of Host Immune Responses. Cambridge University Press, 2004.

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Morrot, Alexandre, ed. Immune Evasion Strategies in Protozoan-Host Interactions. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88966-294-4.

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Book chapters on the topic "Immuno evasione"

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Powers, C., V. DeFilippis, D. Malouli, and K. Früh. "Cytomegalovirus Immune Evasion." In Current Topics in Microbiology and Immunology, 333–59. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-77349-8_19.

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Liang, Chengyu, Hyera Lee, Liguo Wu, Pinghui Feng, and Jae U. Jung. "KSHV Immune Evasion." In DNA Tumor Viruses, 611–44. New York, NY: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-68945-6_24.

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Farrington, Lila, Gabriela O'Neill, and Ann B. Hill. "Viral Immune Evasion." In The Immune Response to Infection, 391–401. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch31.

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Johnson, David C., and Grant McFadden. "Viral Immune Evasion." In Immunology of Infectious Diseases, 357–77. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817978.ch24.

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Mansfield, John M., and Martin Olivier. "Immune Evasion by Parasites." In The Immune Response to Infection, 453–69. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816872.ch36.

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Mansfield, John M., and Martin Olivier. "Immune Evasion by Parasites." In Immunology of Infectious Diseases, 379–92. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817978.ch25.

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Veldkamp, Karin Ellen, and Jos A. G. Strijp. "Innate Immune Evasion by Staphylococci." In Pathogen-Derived Immunomodulatory Molecules, 19–31. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1601-3_2.

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Cohen, Taylor S., Dane Parker, and Alice Prince. "Pseudomonas aeruginosa Host Immune Evasion." In Pseudomonas, 3–23. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9555-5_1.

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Jung, M. Katherine. "Immune Surveillance and Tumor Evasion." In Alcohol and Cancer, 193–210. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4614-0040-0_10.

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Barbosa, Angela S., and Lourdes Isaac. "Complement Immune Evasion by Spirochetes." In Current Topics in Microbiology and Immunology, 215–38. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/82_2017_47.

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Conference papers on the topic "Immuno evasione"

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Damania, Blossom A. "Abstract SY23-01: KSHV: Immune evasion and oncogenesis." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-sy23-01.

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Swanton, Charles. "Abstract IA16: Cancer evolution, immune evasion and metastasis." In Abstracts: AACR Virtual Special Conference on Tumor Heterogeneity: From Single Cells to Clinical Impact; September 17-18, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.tumhet2020-ia16.

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Lane, Ryan S., Julia Femel, Jamie Booth, Christopher Loo, Nicholas Nelson, Takahiro Tsujikawa, Guillaume Thibault, and Amanda W. Lund. "Abstract NG02: Lymphatic vessels: Balancing immune priming and immune evasion in melanoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-ng02.

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Hagan, Christy R., Lauryn Werner, Emma Helm, Margaret Axelrod, Justin Balko, Zachary Hartman, Kent Hunter, Howard Yang, Prabhakar Chalise, and Mary Markiewicz. "Abstract NG15: Progesterone-mediated immune evasion in breast cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-ng15.

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Saigi, Maria, Ryohei Yoshida, Erik H. Knelson, Navin R. Mahadevan, Amir Vajdi, Israel Cañadas, Tran C. Thai, Mark M. Awad, Montse Sánchez-Céspedes, and David A. Barbie. "Abstract 1012: Determinants of immune evasion inMETdriven lung cancer." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-1012.

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Garancher, Alexandra, Hiromichi Suzuki, Svasti Haricharan, Meher B. Masihi, Jessica M. Rusert, Paula S. Norris, Florent Carrette, et al. "Abstract IA11: Overcoming immune evasion in pediatric brain tumors." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-ia11.

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Swanton, Charles. "Abstract IA12: Cancer evolution: Chromosomal instability and immune evasion." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-ia12.

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Christophides, George. "Innate immune response and parasite evasion in malaria vector mosquitoes." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92686.

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Reviriego, Carmen Ballesteros, Anneliese O. Speak, Gemma Turner, Vivek Iyer, Leopold Parts, and David J. Adams. "Abstract B145: Identification of tumor cell intrinsic immune evasion mechanisms." In Abstracts: Fourth CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 30 - October 3, 2018; New York, NY. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr18-b145.

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Giannakis, Marios, Catherine Grasso, Daniel Wells, Tsuyoshi Hamada, Xinmeng Jasmine Mu, Michael Quist, Jonathan Nowak, et al. "Abstract PR03: Genetic mechanisms of immune evasion in colorectal cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-pr03.

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Reports on the topic "Immuno evasione"

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Ma, Feng-Rong, and Gordon Freeman. The Role of PD-1 Ligand in Immune Evasion by Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2005. http://dx.doi.org/10.21236/ada457690.

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Patankar, Manish S. Structural and Functional Analysis of CA125: Potential for Early Diagnosis and Understanding the Immune Evasion Strategies of Epithelial Ovarian Tumors. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada517680.

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Patankar, Manish S. Structural and Functional Analysis of CA125: Potential for Early Diagnosis and Understanding the Immune Evasion Strategies of Epithelial Ovarian Tumors. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada482775.

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Yogev, David, Ricardo Rosenbusch, Sharon Levisohn, and Eitan Rapoport. Molecular Pathogenesis of Mycoplasma bovis and Mycoplasma agalactiae and its Application in Diagnosis and Control. United States Department of Agriculture, April 2000. http://dx.doi.org/10.32747/2000.7573073.bard.

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Mycoplasma bovis and M. agalactiae are two phylogenetically related mycoplasmas which cause economically significant diseases in their respective bovine or small ruminant hosts. These organisms cause persistent asymptomatic infections that can result in severe outbreaks upon introduction of carrier animals into susceptible herds. Little is known about the mechanisms underlying mycoplasma-host interaction, variation in virulence, or of the factors enabling avoidance of the host immune system. In recent years it has become apparent that the ability of pathogenic microorganisms to rapidly alter surface antigenic structures and to fine tune their antigenicity, a phenomena called antigenic variation, is one of the most effective strategies used to escape immune destruction and to establish chronic infections. Our discovery of a novel genetic system, mediating antigenic variation in M. bovis (vsp) as well as in M. agalactiae (avg) served as a starting point for our proposal which included the following objectives: (i) Molecular and functional characterization of the variable surface lipoproteins (Vsp) system of M. bovis and comparison with the Vsp-counterpart in M. agalactiae (ii) Determination of the role of Vsp proteins in the survival of M. bovis when confronted by host defense factors, (iii) Assessment of Vsp-based genetic and antigenic typing of M. bovis and M. agalactiae for epidemiology of infection and (iv) Improvement of diagnostic tests for M. bovis and M. agalactiae based on the vsp-and vsp-analogous systems. We have carried out an extensive molecular characterization of the vsp system and unravelled the precise molecular mechanism responsible for the generation of surface antigenic variation in M. bovis. Our data clearly demonstrated that the two pathogenic mycoplasma species possess large gene families encoding variable lipoprotein antigens that apparently play an important role in immune evasion and in pathogen-host interaction during infection. Phase variable production of these antigens was found to be mediated by a novel molecular mechanism utilizing double site-specific DNA inversions via an intermediate vsp configuration. Studies in model systems indicate that phase variation of VspA is relevant in interaction between M. bovis and macrophages or monocytes, a crucial stage in pathogenesis. Using an ELISA test with captured VspA as an antigen, phase variation was shown to occur in vivo and under field conditions. Genomic rearrangements in the avg gene family of M. agalactiae were shown to occur in vivo and may well have a role in evasion of host defences and establishment of chronic infection. An epidemiological study indicated that patterns of vsp-related antigenic variation diverge rapidly in an M. bovis infected herd. Marked divergence was also found with avg-based genomic typing of M. agalactiae in chronically infected sheep. However, avg-genomic fingerprints were found to be relatively homogeneous in different animals during acute stages of an outbreak of Contagious Agalactiae, and differ between unrelated outbreaks. These data support the concept of vsp-based genomic typing but indicate the necessity for further refinement of the methodology. The molecular knowledge on these surface antigens and their encoding genes provides the basis for generating specific recombinant tools and serological methods for serodiagnosis and epidemiological purposes. Utilization of these methods in the field may allow differentiating acutely infected herds from chronic herds and disease-free herds. In addition the highly immunogenic nature of these lipoproteins may facilitate the design of protective vaccine against mycoplasma infections.
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Eldar, Avigdor, and Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.

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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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