Relevant bibliographies by topics / Innate immune signalling

Academic literature on the topic 'Innate immune signalling'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Innate immune signalling"

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Guillamot, Maria, and Iannis Aifantis. "Splicing the innate immune signalling in leukaemia." Nature Cell Biology 21, no. 5 (April 22, 2019): 536–37. http://dx.doi.org/10.1038/s41556-019-0323-4.

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Yu, Xiaoyu, Liyuan Zhang, Jingxiang Shen, Yanfang Zhai, Qifei Jiang, Mengran Yi, Xiaobing Deng, et al. "The STING phase-separator suppresses innate immune signalling." Nature Cell Biology 23, no. 4 (April 2021): 330–40. http://dx.doi.org/10.1038/s41556-021-00659-0.

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Weidenbusch, Marc, Onkar P. Kulkarni, and Hans-Joachim Anders. "The innate immune system in human systemic lupus erythematosus." Clinical Science 131, no. 8 (March 28, 2017): 625–34. http://dx.doi.org/10.1042/cs20160415.

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Although the role of adaptive immune mechanisms, e.g. autoantibody formation and abnormal T-cell activation, has been long noted in the pathogenesis of human systemic lupus erythematosus (SLE), the role of innate immunity has been less well characterized. An intricate interplay between both innate and adaptive immune elements exists in protective anti-infective immunity as well as in detrimental autoimmunity. More recently, it has become clear that the innate immune system in this regard not only starts inflammation cascades in SLE leading to disease flares, but also continues to fuel adaptive immune responses throughout the course of the disease. This is why targeting the innate immune system offers an additional means of treating SLE. First trials assessing the efficacy of anti-type I interferon (IFN) therapy or modulators of pattern recognition receptor (PRR) signalling have been attempted. In this review, we summarize the available evidence on the role of several distinct innate immune elements, especially neutrophils and dendritic cells as well as the IFN system, as well as specific innate PRRs along with their signalling pathways. Finally, we highlight recent clinical trials in SLE addressing one or more of the aforementioned components of the innate immune system.
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Hopcraft, Sharon E., and Blossom Damania. "Tumour viruses and innate immunity." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1732 (September 11, 2017): 20160267. http://dx.doi.org/10.1098/rstb.2016.0267.

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Host cells sense viral infection through pattern recognition receptors (PRRs), which detect pathogen-associated molecular patterns (PAMPs) and stimulate an innate immune response. PRRs are localized to several different cellular compartments and are stimulated by viral proteins and nucleic acids. PRR activation initiates signal transduction events that ultimately result in an inflammatory response. Human tumour viruses, which include Kaposi's sarcoma-associated herpesvirus, Epstein–Barr virus, human papillomavirus, hepatitis C virus, hepatitis B virus, human T-cell lymphotropic virus type 1 and Merkel cell polyomavirus, are detected by several different PRRs. These viruses engage in a variety of mechanisms to evade the innate immune response, including downregulating PRRs, inhibiting PRR signalling, and disrupting the activation of transcription factors critical for mediating the inflammatory response, among others. This review will describe tumour virus PAMPs and the PRRs responsible for detecting viral infection, PRR signalling pathways, and the mechanisms by which tumour viruses evade the host innate immune system. This article is part of the themed issue ‘Human oncogenic viruses’.
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Triantafilou, Martha, Philipp M. Lepper, Robin Olden, Ivo de Seabra Rodrigues Dias, and Kathy Triantafilou. "Location, Location, Location: Is Membrane Partitioning Everything When It Comes to Innate Immune Activation?" Mediators of Inflammation 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/186093.

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In the last twenty years, the general view of the plasma membrane has changed from a homogeneous arrangement of lipids to a mosaic of microdomains. It is currently thought that islands of highly ordered saturated lipids and cholesterol, which are laterally mobile, exist in the plane of the plasma membrane. Lipid rafts are thought to provide a means to explain the spatial segregation of certain signalling pathways emanating from the cell surface. They seem to provide the necessary microenvironment in order for certain specialised signalling events to take place, such as the innate immune recognition. The innate immune system seems to employ germ-lined encoded receptors, called pattern recognition receptors (PRRs), in order to detect pathogens. One family of such receptors are the Toll-like receptors (TLRs), which are the central “sensing” apparatus of the innate immune system. In recent years, it has become apparent that TLRs are recruited into membrane microdomains in response to ligands. These nanoscale assemblies of sphingolipid, cholesterol, and TLRs stabilize and coalesce, forming signalling platforms, which transduce signals that lead to innate immune activation. In the current paper, we will investigate all past and current literature concerning recruitment of extracellular and intracellular TLRs into lipid rafts and how this membrane organization modulates innate immune responses.
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Eades, Lauren, Michael Drozd, and Richard M. Cubbon. "Hypoxia signalling in the regulation of innate immune training." Biochemical Society Transactions 50, no. 1 (January 11, 2021): 413–22. http://dx.doi.org/10.1042/bst20210857.

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Innate immune function is shaped by prior exposures in a phenomenon often referred to as ‘memory’ or ‘training’. Diverse stimuli, ranging from pathogen-associated molecules to atherogenic lipoproteins, induce long-lasting training, impacting on future responses, even to distinct stimuli. It is now recognised that epigenetic modifications in innate immune cells, and their progenitors, underpin these sustained behavioural changes, and that rewired cellular metabolism plays a key role in facilitating such epigenetic marks. Oxygen is central to cellular metabolism, and cells exposed to hypoxia undergo profound metabolic rewiring. A central effector of these responses are the hypoxia inducible factors (or HIFs), which drive transcriptional programmes aiming to adapt cellular homeostasis, such as by increasing glycolysis. These metabolic shifts indirectly promote post-translational modification of the DNA-binding histone proteins, and also of DNA itself, which are retained even after cellular oxygen tension and metabolism normalise, chronically altering DNA accessibility and utilisation. Notably, the activity of HIFs can be induced in some normoxic circumstances, indicating their broad importance to cell biology, irrespective of oxygen tension. Some HIFs are implicated in innate immune training and hypoxia is present in many disease states, yet many questions remain about the association between hypoxia and training, both in health and disease. Moreover, it is now appreciated that cellular responses to hypoxia are mediated by non-HIF pathways, suggesting that other mechanisms of training may be possible. This review sets out to define what is already known about the topic, address gaps in our knowledge, and provide recommendations for future research.
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Boudsocq, Marie, Matthew R. Willmann, Matthew McCormack, Horim Lee, Libo Shan, Ping He, Jenifer Bush, Shu-Hua Cheng, and Jen Sheen. "Differential innate immune signalling via Ca2+ sensor protein kinases." Nature 464, no. 7287 (February 17, 2010): 418–22. http://dx.doi.org/10.1038/nature08794.

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Zhang, Yaxing, Zan Huang, and Hongliang Li. "Insights into innate immune signalling in controlling cardiac remodelling." Cardiovascular Research 113, no. 13 (July 3, 2017): 1538–50. http://dx.doi.org/10.1093/cvr/cvx130.

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Shadel, Gerald S. "Mitochondrial DNA stress in innate immune signalling and cancer." Biochimica et Biophysica Acta (BBA) - Bioenergetics 1857 (August 2016): e5-e6. http://dx.doi.org/10.1016/j.bbabio.2016.04.408.

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Sprenger, Hans-Georg, Thomas MacVicar, Amir Bahat, Kai Uwe Fiedler, Steffen Hermans, Denise Ehrentraut, Katharina Ried, et al. "Cellular pyrimidine imbalance triggers mitochondrial DNA–dependent innate immunity." Nature Metabolism 3, no. 5 (April 26, 2021): 636–50. http://dx.doi.org/10.1038/s42255-021-00385-9.

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AbstractCytosolic mitochondrial DNA (mtDNA) elicits a type I interferon response, but signals triggering the release of mtDNA from mitochondria remain enigmatic. Here, we show that mtDNA-dependent immune signalling via the cyclic GMP–AMP synthase‒stimulator of interferon genes‒TANK-binding kinase 1 (cGAS–STING–TBK1) pathway is under metabolic control and is induced by cellular pyrimidine deficiency. The mitochondrial protease YME1L preserves pyrimidine pools by supporting de novo nucleotide synthesis and by proteolysis of the pyrimidine nucleotide carrier SLC25A33. Deficiency of YME1L causes inflammation in mouse retinas and in cultured cells. It drives the release of mtDNA and a cGAS–STING–TBK1-dependent inflammatory response, which requires SLC25A33 and is suppressed upon replenishment of cellular pyrimidine pools. Overexpression of SLC25A33 is sufficient to induce immune signalling by mtDNA. Similarly, depletion of cytosolic nucleotides upon inhibition of de novo pyrimidine synthesis triggers mtDNA-dependent immune responses in wild-type cells. Our results thus identify mtDNA release and innate immune signalling as a metabolic response to cellular pyrimidine deficiencies.
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Dissertations / Theses on the topic "Innate immune signalling"

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Watkinson, Ruth Elizabeth. "Intracellular antibody receptor TRIM21 in viral neutralisation and innate immune signalling." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708305.

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Schreuder, Lisa Jane. "Effects of Mycrobacteria on the Signalling Machinenary of Bovine Innate Immune Cells." Thesis, Royal Veterinary College (University of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.499275.

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Jan, Afnan. "A role for connexin signalling in the innate immune response in the skin." Thesis, Glasgow Caledonian University, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.726766.

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Bilkei-Gorzo, Orsolya. "Ubiquitylation regulates vesicle trafficking and innate immune responses on the phagosome of inflammatory macrophages." Thesis, University of Dundee, 2018. https://discovery.dundee.ac.uk/en/studentTheses/8661922d-9d5e-4a4a-bfd4-b0f5e5717c61.

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Macrophages are sentinels present in most tissues of the body, where they recognise and respond to biological dangers. Recognition and uptake of particles is mediated through phagocytic receptors which upon activation induce appropriate responses. These responses need to be tightly regulated in order to destroy pathogens but prevent uncontrolled inflammation. Phagocytosis is an evolutionarily conserved process required for host defence and homeostasis. During phagocytosis, particles are recognised by cell surface receptors that trigger rearrangement of the actin cytoskeleton and internalization of the bound particle into a de novo, membranous organelle known as the phagosome. Regulation of phagocytosis and phagosome maturation can be achieved through changes in transcription/translation and differential recruitment of proteins but also through their non-translational modifications. Here I explored the role of ubiquitylation in the phagosome biogenesis of Interferon-gamma (IFN-ɣ) activated macrophages. Ubiquitylation is a diverse, reversible post-translational modification which is not only involved in protein degradation but also in vesicle trafficking and immune signalling. My data shows that phagosomes are enriched in polyubiquitylation, which is further enhanced by IFN-ɣ. I applied a targeted AQUA peptide approach by which we quantified ubiquitin chain linkage peptides from phagosome samples by PRM. This data shows that all chain linkages apart from M1/linear chains are present on phagosomes. Furthermore, IFN-ɣ activation enhanced K11, K48 and K63 chains significantly. In order to identify the molecular function of this polyubiquitylation, I characterized the ubiquitinome of phagosomes of IFN-γ activated macrophages and can demonstrate that ubiquitylation is preferentially attached to proteins involved in vesicle trafficking, thereby delaying fusion with late endosomes and lysosomes. I demonstrated that most ubiquitin chains are on the cytoplasmic site of the phagosome enabling an interaction of ubiquitin chains with cytosolic proteins such as Rab7. Rab7 a major regulator of vesicle trafficking could be shown to be ubiquitylated on phagosomes. I further showed that phagosomal recruitment of the E3 ligase RNF115 is enhanced upon IFN-γ stimulation and RNF115 is responsible for most of the increase of K63 polyubiquitylation of phagosomal proteins. Knock-down of RNF115 promotes phagosome maturation and induces an increased pro-inflammatory response to Toll-like receptor (TLR) agonists, indicating that RNF115 is a negative regulator of vesicular trafficking to the lysosome and disruption of this pathway induces pro-inflammatory responses in macrophages. In conclusion, this is the first study showing unbiasedly that ubiquitylation plays an important role in vesicle trafficking to the lysosome.
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Gaughan, Daniel. "The role of DNA damage response proteins in innate immune signalling : a new role for BRCA1." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:252f589f-40c0-4f7f-be3d-124e588e92a8.

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Pattern Recognition Receptors (PRRs), which have evolved to detect a diverse array of pathogenic features known as Pathogen Associated Molecular Patterns (PAMPs), are localised optimally for interaction with their cognate ligands. Upon Receptor activation, signal transduction pathways are induced which converge at different points to direct a specific inflammatory response. TBK1 is activated and recruited to multiple PRRs, where it in turn recruits and phosphorylates IRF3 which then translocates to the nucleus and induces the expression of type I IFN. In this study, the major breast cancer susceptibility protein BRCA1, known for its functional role in maintaining genomic stability, is found to be phosphorylated following PRR triggering. This event is demonstrated to be DNA Damage, DNA Damage Response (DDR) signalling, and oxidative stress-independent. Further to this, phosphorylated BRCA1 localises to Golgi-related microsomes in perinuclear zones where TBK1 and the adaptor STING can be found. Here, BRCA1 interacts biochemically with and facilitates full activation of TBK1. BRCA1-deficient cells show abrogated IRF3 phosphorylation, type I IFN production and ISG induction in response to a diverse array of PRR agonists as well as both HSV1 and Sendaï virus (SeV). Subsequently, BRCA1 deficiency impairs antiviral responses to pathogens such as HSV1.
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Homem, Rafael Augusto. "Redox signalling and innate immunity : a role for protein S-nitrosylation in the immune response of Drosophila melanogaster." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/15971.

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Over the past three decades, nitric oxide (NO) has been recognised as one of the most versatile and important players in many aspects of physiology, including immune responses. More recently, S-nitrosylation, the incorporation of a NO moiety into a protein thiol group, has emerged as a major post-translational modification (PTM) during pathophysiological responses in plants and animals. The main goal of this work was to investigate the role of S-nitrosylation in physiology and innate immunity of animals using the genetic reference system, Drosophila melanogaster. The S-nitrosylated derivative of glutathione (GSH), S-nitrosoglutathione (GSNO), is the main non-protein S-nitrosothiol (SNO) in the cell and extracellular fluids. GSNO can trans-S-nitrosylate other thiols and is considered a reservoir of NO bioactivity. The levels of GSNO and total S-nitrosylation have been shown to be controlled by S-nitrosoglutathione reductase (GSNOR) in yeast, plants and mammals. By employing an overlapping deletion technique to knock-out gsnor, a role for S-nitrosylation in the immune response of D. melanogaster is proposed. Compared to wild type flies, gsnor overlapping deletion flies presented lower expression of antimicrobial peptides in response to infections, and succumbed more rapidly to both Gram-positive bacterial and fungal pathogens. As the Toll pathway mediates responses against these pathogens, key components of this network were tested for their propensity to being S-nitrosylated. Two CLIP-domain serine proteases of the Toll signalling pathway, Persephone (PSH) and Spätzle-Processing Enzyme (SPE), were shown to be S-nitrosylated both in vitro and in vivo and this process seemed to control the quaternary structure of these proteins and interfere with the immune response of D. melanogaster. At least for PSH, S-nitrosylation at C254 has an immune significance as the expression of non-Snitrosylable PSHC254S in gsnor knock-out flies partially recovered the resistance of these animals to infections with the entomopathogenic fungus Beauveria bassiana. These findings might represent a novel mechanism by which NO and S-nitrosylation regulate immunity. Further results presented in this thesis reveal an interplay between reactive oxygen species (ROS) and reactive nitrogen species (RNS) in D. melanogaster physiology and immunity. Similarly to what has been reported in Arabidopsis thaliana, gsnor knock-out flies presented higher tolerance to the herbicide paraquat, an inducer of superoxide (O2 -) production. Moreover, additional mutations in Catalase (Cat), a hydrogen peroxide (H2O2) scavenger enzyme, partially restored the immunodeficiency phenotypes of gsnor knock-out flies. These findings suggest an inter-relation between the levels of ROS and RNS during stress responses of plants and animals. In addition, CRISPR/Cas9 technology was employed to generate gsnor knock-outs in the genome of D. melanogaster. These flies were shown to have no GSNOR activity, presented lower tolerance to pharmacological-induced nitrosative stress and succumbed faster to infections with B. bassiana compared to wild type flies. These results support the role played by GSNOR in regulating NO homeostasis and immunity in D. melanogaster.
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Reder, Gabor. "Development of a phosphoproteomic screen of innate immune signalling : identification and characterisation of a novel phosphorylation of NFkB1/p105." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/6150.

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Toll-like receptors (TLRs) expressed by antigen-presenting cells of the innate immune system, such as macrophages, detect microbial products and activate signalling cascades that initiate specific gene expression programmes that define the subsequent adaptive immune response. However, it is poorly understood how TLR-specific responses arise, as many of the signalling components are common to multiple TLRs, and it is likely that as yet undiscovered phosphorylations of signalling proteins contribute to specificity of TLR pathways. TLR4, the receptor for lipopolysaccharide (LPS), is used as a model system for TLR signalling, as it activates many of the signalling mechanisms utilised by other TLRs, and I attempted to discover novel regulatory phosphorylations in LPS-activated RAW 264.7 macrophages. Because it is not yet possible to accurately predict post-translational modifications from genomic data, the exact sites of phosphorylation have to be identified experimentally, and the method of choice for this is mass spectrometry-based phosphoproteomics. Using an optimised phosphoproteomics workflow and stringent filtering criteria, I identified 445 phosphorylation sites in unstimulated and LPS-treated RAW macrophages, several of which were potential LPS-induced regulatory phosphorylations, including a previously uncharacterised phosphorylation of the NF-κB protein p105, a key regulator of TLR and other inflammatory signalling pathways. Following validation of a phospho-specific p105 antibody, I demonstrated that the novel phosphorylation of p105 was induced by LPS, other TLR ligands, tumour necrosis factor (TNF)-α, and prostaglandin E2 in RAW macrophages and primary human macrophages, and by interleukin (IL)-1β in 4 primary human skin fibroblasts. Moreover, the LPS-induced phosphorylation of p105 was blocked by the protein kinase A (PKA) inhibitor H89. These results indicate that the novel phosphorylation of p105 may be important for the regulation of TLR and other inflammatory signalling pathways in both hemopoietic and non-hemopoietic cells.
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Anselm, Bettina [Verfasser], and Bianca [Akademischer Betreuer] Schaub. "Early priming of the immune system: Identifying predictive markers of innate immunity and calcium signalling for the development of asthma / Bettina Anselm ; Betreuer: Bianca Schaub." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1204827915/34.

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Westphal, Andreas [Verfasser], Kyeong-Hee [Akademischer Betreuer] Lee, Norbert [Akademischer Betreuer] Reiling, and Georgios [Akademischer Betreuer] Tsiavaliaris. "Lysosomal trafficking regulator Lyst controls innate immune cell signalling and function : regulation of TLR-mediated TRIF signalling and control of mast cell-mediated allergic reactions / Andreas Westphal ; Akademische Betreuer: Kyeong-Hee Lee, Norbert Reiling, Georgios Tsiavaliaris ; Institut für Klinische Chemie." Hannover : Bibliothek der Medizinischen Hochschule Hannover, 2017. http://d-nb.info/1143981758/34.

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Czerwińska, Urszula. "Unsupervised deconvolution of bulk omics profiles : methodology and application to characterize the immune landscape in tumors Determining the optimal number of independent components for reproducible transcriptomic data analysis Application of independent component analysis to tumor transcriptomes reveals specific and reproducible immune-related signals A multiscale signalling network map of innate immune response in cancer reveals signatures of cell heterogeneity and functional polarization." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB075.

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Les tumeurs sont entourées d'un microenvironnement complexe comprenant des cellules tumorales, des fibroblastes et une diversité de cellules immunitaires. Avec le développement actuel des immunothérapies, la compréhension de la composition du microenvironnement tumoral est d'une importance critique pour effectuer un pronostic sur la progression tumorale et sa réponse au traitement. Cependant, nous manquons d'approches quantitatives fiables et validées pour caractériser le microenvironnement tumoral, facilitant ainsi le choix de la meilleure thérapie. Une partie de ce défi consiste à quantifier la composition cellulaire d'un échantillon tumoral (appelé problème de déconvolution dans ce contexte), en utilisant son profil omique de masse (le profil quantitatif global de certains types de molécules, tels que l'ARNm ou les marqueurs épigénétiques). La plupart des méthodes existantes utilisent des signatures prédéfinies de types cellulaires et ensuite extrapolent cette information à des nouveaux contextes. Cela peut introduire un biais dans la quantification de microenvironnement tumoral dans les situations où le contexte étudié est significativement différent de la référence. Sous certaines conditions, il est possible de séparer des mélanges de signaux complexes, en utilisant des méthodes de séparation de sources et de réduction des dimensions, sans définitions de sources préexistantes. Si une telle approche (déconvolution non supervisée) peut être appliquée à des profils omiques de masse de tumeurs, cela permettrait d'éviter les biais contextuels mentionnés précédemment et fournirait un aperçu des signatures cellulaires spécifiques au contexte. Dans ce travail, j'ai développé une nouvelle méthode appelée DeconICA (Déconvolution de données omiques de masse par l'analyse en composantes immunitaires), basée sur la méthodologie de séparation aveugle de source. DeconICA a pour but l'interprétation et la quantification des signaux biologiques, façonnant les profils omiques d'échantillons tumoraux ou de tissus normaux, en mettant l'accent sur les signaux liés au système immunitaire et la découverte de nouvelles signatures. Afin de rendre mon travail plus accessible, j'ai implémenté la méthode DeconICA en tant que librairie R. En appliquant ce logiciel aux jeux de données de référence, j'ai démontré qu'il est possible de quantifier les cellules immunitaires avec une précision comparable aux méthodes de pointe publiées, sans définir a priori des gènes spécifiques au type cellulaire. DeconICA peut fonctionner avec des techniques de factorisation matricielle telles que l'analyse indépendante des composants (ICA) ou la factorisation matricielle non négative (NMF). Enfin, j'ai appliqué DeconICA à un grand volume de données : plus de 100 jeux de données, contenant au total plus de 28 000 échantillons de 40 types de tumeurs, générés par différentes technologies et traités indépendamment. Cette analyse a démontré que les signaux immunitaires basés sur l'ICA sont reproductibles entre les différents jeux de données. D'autre part, nous avons montré que les trois principaux types de cellules immunitaires, à savoir les lymphocytes T, les lymphocytes B et les cellules myéloïdes, peuvent y être identifiés et quantifiés. Enfin, les métagènes dérivés de l'ICA, c'est-à-dire les valeurs de projection associées à une source, ont été utilisés comme des signatures spécifiques permettant d'étudier les caractéristiques des cellules immunitaires dans différents types de tumeurs. L'analyse a révélé une grande diversité de phénotypes cellulaires identifiés ainsi que la plasticité des cellules immunitaires, qu'elle soit dépendante ou indépendante du type de tumeur. Ces résultats pourraient être utilisés pour identifier des cibles médicamenteuses ou des biomarqueurs pour l'immunothérapie du cancer
Tumors are engulfed in a complex microenvironment (TME) including tumor cells, fibroblasts, and a diversity of immune cells. Currently, a new generation of cancer therapies based on modulation of the immune system response is in active clinical development with first promising results. Therefore, understanding the composition of TME in each tumor case is critically important to make a prognosis on the tumor progression and its response to treatment. However, we lack reliable and validated quantitative approaches to characterize the TME in order to facilitate the choice of the best existing therapy. One part of this challenge is to be able to quantify the cellular composition of a tumor sample (called deconvolution problem in this context), using its bulk omics profile (global quantitative profiling of certain types of molecules, such as mRNA or epigenetic markers). In recent years, there was a remarkable explosion in the number of methods approaching this problem in several different ways. Most of them use pre-defined molecular signatures of specific cell types and extrapolate this information to previously unseen contexts. This can bias the TME quantification in those situations where the context under study is significantly different from the reference. In theory, under certain assumptions, it is possible to separate complex signal mixtures, using classical and advanced methods of source separation and dimension reduction, without pre-existing source definitions. If such an approach (unsupervised deconvolution) is feasible to apply for bulk omic profiles of tumor samples, then this would make it possible to avoid the above mentioned contextual biases and provide insights into the context-specific signatures of cell types. In this work, I developed a new method called DeconICA (Deconvolution of bulk omics datasets through Immune Component Analysis), based on the blind source separation methodology. DeconICA has an aim to decipher and quantify the biological signals shaping omics profiles of tumor samples or normal tissues. A particular focus of my study was on the immune system-related signals and discovering new signatures of immune cell types. In order to make my work more accessible, I implemented the DeconICA method as an R package named "DeconICA". By applying this software to the standard benchmark datasets, I demonstrated that DeconICA is able to quantify immune cells with accuracy comparable to published state-of-the-art methods but without a priori defining a cell type-specific signature genes. The implementation can work with existing deconvolution methods based on matrix factorization techniques such as Independent Component Analysis (ICA) or Non-Negative Matrix Factorization (NMF). Finally, I applied DeconICA to a big corpus of data containing more than 100 transcriptomic datasets composed of, in total, over 28000 samples of 40 tumor types generated by different technologies and processed independently. This analysis demonstrated that ICA-based immune signals are reproducible between datasets and three major immune cell types: T-cells, B-cells and Myeloid cells can be reliably identified and quantified. Additionally, I used the ICA-derived metagenes as context-specific signatures in order to study the characteristics of immune cells in different tumor types. The analysis revealed a large diversity and plasticity of immune cells dependent and independent on tumor type. Some conclusions of the study can be helpful in identification of new drug targets or biomarkers for immunotherapy of cancer
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Books on the topic "Innate immune signalling"

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Geri, Guillaume, and Jean-Paul Mira. Host–pathogen interactions in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0306.

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Infection by a pathogenic micro-organism triggers a coordinated activation of both innate and adaptive immune responses. The innate immune response quickly triggers an antimicrobial response that will initiate development of a pathogen-specific, long-lasting adaptive immune response. Accurate recognition of microbial-associated molecular patterns by pattern-recognition receptors (PRRs) is the cornerstone of this immediate response. Most studied PRRs are Toll-like receptors (TLRs) and their kinase signalling cascades that activate nuclear transcription factors, and induce gene expression and cytokine production. Deficiencies or genetic variability in these different signalling pathways may lead to recurrent pyogenic infections and severe invasive diseases. After initial contact between the host and pathogen, numerous factors mediate the inflammatory response, as pro-inflammatory cytokines and chemokines. Apart from host genetic variability, pathogen diversity also influences the phenotypic features of various infectious diseases. Genomic analysis may assist in the development of targeted therapies or new therapeutic strategies based on both patient and microorganism genotype.
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Monaco, Claudia, and Giuseppina Caligiuri. Molecular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0014.

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The development of the atherosclerotic plaque relies on specific cognate interactions between ligands and receptors with the ability to regulate cell recruitment, inflammatory signalling, and the production of powerful inflammatory and bioactive lipid mediators. This chapter describes how signalling is engaged by cell-cell surface interactions when the endothelium interacts with platelets and leukocytes enhancing leukocyte recruitment during atherogenesis. It also exemplifies intracellular signalling pathways induced by the activation of innate immune receptors, the most potent activators of inflammation in physiology and disease. Differences are highlighted in innate signalling pathways in metabolic diseases such as atherosclerosis compared to canonical immunological responses. Finally, the key lipid mediators whose production can affect endothelial function, inflammation, and atherosclerosis development are summarized. This Chapter will take you through these fundamental steps in the development of the atherosclerotic plaque by summarizing very recent knowledge in the field and highlighting recent or ongoing clinical trials that may enrich our ability to target cardiovascular disease in the future.
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Winchester, Robert, Darren D. O’Rielly, and Proton Rahman. Genetics of psoriatic arthritis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198737582.003.0006.

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The psoriatic phenotype is clinically heterogeneous with psoriatic arthritis (PsA) itself being heterogeneous. Studies have consistently demonstrated that PsA has a strong genetic component and disease pathogenesis encompasses a complex interplay between genetic, immunological, and environmental factors. In this chapter, we will review the genetics of PsA including the major histocompatibility complex (MHC) region and non-MHC loci. We will detail how susceptibility genes can be grouped into barrier integrity, innate immune response, and adaptive immune response (particularly Th-17 lymphocyte signalling). We will articulate how these studies strongly support PsA as genetically different from PsV and that the genetic heterogeneity is likely attributed to different HLA susceptibility alleles within the MHC region that an individual carries. Furthermore, we will highlight new emerging technologies, in particular, next-generation sequencing, which may lead to new genetic discoveries in PsA.
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Book chapters on the topic "Innate immune signalling"

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Mulhern, Orla, Barry Harrington, and Andrew G. Bowie. "Modulation of Innate Immune Signalling Pathways by Viral Proteins." In Pathogen-Derived Immunomodulatory Molecules, 49–63. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-1601-3_4.

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Galvão, Izabela, Lirlândia P. Sousa, Mauro M. Teixeira, and Vanessa Pinho. "PI3K Isoforms in Cell Signalling and Innate Immune Cell Responses." In Current Topics in Microbiology and Immunology, 147–64. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-06566-8_6.

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Kuraishi, Takayuki, Hirotaka Kanoh, Yoshiki Momiuchi, Hiroyuki Kenmoku, and Shoichiro Kurata. "The Drosophila Toll Pathway: A Model of Innate Immune Signalling Activated by Endogenous Ligands." In Chronic Inflammation, 119–29. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56068-5_10.

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Schmid-Hempel, Paul. "The natural history of defences." In Evolutionary Parasitology, 51–108. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780198832140.003.0004.

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Hosts can avoid infections by behavioural changes and by body walls. After infection, hosts can change their behaviours to reduce the effects of parasitism. Immune defences have different arms (humoral or cellular), and organization (innate, adaptive). Innate immunity consists of a collection of different systems that are evolutionarily very old. Adaptive immunity, based on expansion of specific lymphocytes, evolved in the higher vertebrates. Immune defences are regulated tightly and based on receptors that can recognize parasites (or their activity). This triggers a complex signalling cascade that results in the production of further signalling compounds and effectors. Important protein families, e.g. the immunoglobulins, form the molecular backbone. A key to efficient defences is the diversification of receptors, such as the highly evolved somatic diversification processes of advanced adaptive immunity. The microbiota adds to defences in many ways. Immune memory and priming occur throughout the tree of life.
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Marina Andrei, Ana, Elena Cristina Andrei, Elena Camelia Stănciulescu, Mihaela Cezarina Mehedinți, Mihaela Jana Țuculină, Ileana Monica Baniță, Sandra Alice Buteică, and Cătălina Gabriela Pisoschi. "Innate Immune Response as a New Challenge in Periodontal Inflammation." In Periodontology - Fundamentals and Clinical Features [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96801.

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Gingivitis and periodontitis are induced by numerous pathogenic microbiota hosted in the subgingival biofilm that first trigger the innate immune response. Innate immune response is part of a homeostatic system which is the first line defence and defines the host inherited resistance to infection. Both genetic and environmental factors are involved in variable individual susceptibility to inflammation of periodontal tissues. That is why, although more than 600 bacterial species have been detected in the periodontal plaque, the type of bacteria incriminated in the development of the inflammation is still unclear. Moreover, in the last decade gene polymorphisms have been largely recognised as important conditions associated with increased susceptibility to periodontal diseases. Manipulating the immune response by the development of drugs that inhibit adverse host reactions and promote beneficial effects might be of therapeutic or prophylactic importance. This work intends to assess the importance of Toll-like receptors as main effectors of the innate immune response in the triggering, maintenance and progression of periodontal inflammation, as well as of the involvement of synthetic molecules targeting TLR signalling pathways in treating periodontal diseases.
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Kumar, Jitendra, Priya Sharma, Murli Dhar Mitra, Sonia Sangwan, and Haribrahma Singh. "Molecular Impact of Dietary Fibre Metabolites on Intestinal Immunity of Host." In Immunology of the GI Tract - Recent Advances. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.107348.

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Food contains several components that are essential for health. Dietary fibres are nondigestible foods that play an important role in the maintenance of health. Nondigestible carbohydrates are an important constituent of the diet. Intestinal immunity is the bedrock of host health and holistic health maintained by nutrition and the existence of the host supported by immunity. The gastrointestinal immune barrier is exposed to the environment or food, and immunity is maintained by several factors. Dietary fibres exert molecular effects through the production of short-chain fatty acids (SCFAs) and gut microbiota. Dietary fibres and microbial communities secrete metabolites that have the potential to regulate intestinal immunity. The gastrointestinal immune barrier is a primary target for dietary fibre metabolites, and these molecules exert a signalling effect on immune cells in the intestine. In the proposed chapter, we will discuss the molecular impact of dietary fibers on intestinal immunity and how innate immune response and gut microbiota are regulated by metabolites.
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Distler, Oliver, and Caroline Ospelt. "Rheumatoid arthritis: basic mechanisms in joints." In ESC CardioMed, 1109–12. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0271.

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Rheumatoid arthritis (RA) is a destructive polyarthritis which mostly starts in the small joints of the hands and feet. In the course of the disease, more proximal joints also become involved. The progressive destruction of joint structures is mediated by the chronically inflamed, hyperplasic synovial tissue, which attaches to and degrades the adjacent joint cartilage. Typical changes of the RA synovium are increased cellularity in the synovial lining and sublining layer, including vascularization, giant cell formation, and immigration of immune cells. The inflammatory cell infiltrate comprises macrophages, monocytes, dendritic cells, T cells, B cells, plasma cells, innate lymphoid cells, and mast cells. These cells together with resident stromal cells (synovial fibroblasts) form a complex network and maintain inflammatory and destructive processes via the secretion of various cytokines and chemokines. Intracellularly, cytokine-activated receptor signalling is mediated via protein kinase-dependent signalling pathways, such as mitogen-activated protein kinases and Janus kinase, which leads to the activation of transcription factors and thus changes in the transcriptional programme. Gene transcription is additionally modified by epigenetic mechanisms and post-transcriptionally by microRNA.
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Sundar, Kothandapani, Ramachandira Prabu, and Gopal Jayalakshmi. "Quorum Sensing Inhibition Based Drugs to Conquer Antimicrobial Resistance." In The Global Antimicrobial Resistance Epidemic - Innovative Approaches and Cutting-Edge Solutions [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104125.

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Quorum sensing is the cell to cell communication mechanism in microorganism through signalling molecules. Regulation of virulence factor, sporulation, proteolytic enzymes production, biofilm formation, auto-inducers, cell population density are key physiological process mediated through quorum-sensing (QS) signalling. Elevation of innate immune system and antibiotic tolerance of pathogens is highly increased with perspective of quorum-sensing (QS) activity. Development of novel drugs is highly attractive scenario against cell-cell communication of microbes. Design of synthetic drugs and natural compounds against QS signal molecules is vital combat system to attenuate microbial pathogenicity. Quorum sensing inhibitors (QSIs), quorum quenchers (QQs), efflux pump inhibitors (EPIs) act against multi-drug resistance strains (MDR) and other pathogenic microbes through regulation of auto-inducers and signal molecule with perceptive to growth arrest both in-vitro and in-vivo. QQs, QSIs and EPIs compounds has been validated with various animal models for high selection pressure on therapeutics arsenal against microbe’s growth inhibition. Promising QSI are phytochemicals and secondary metabolites includes polyacetylenes, alkaloids, polyphenols, terpenoids, quinones.
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Gomperts, Bastien D., IJsbrand M. Kramer, and Peter E. R. Tatham. "Activation of the Innate immune System: The Toll-like Receptor 4 and Signalling through Ubiquitylation." In Signal Transduction, 451–82. Elsevier, 2009. http://dx.doi.org/10.1016/b978-0-12-369441-6.00015-5.

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Conference papers on the topic "Innate immune signalling"

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Marcec, Matthew. "Calcium and ROS signalling in plant innate immune responses." In ASPB PLANT BIOLOGY 2020. USA: ASPB, 2020. http://dx.doi.org/10.46678/pb.20.1053034.

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Luo, X., M. Lu, HA Baba, G. Gerken, H. Wedemeyer, and R. Broering. "The Hippo signalling is induced by Toll-like receptor 4 activation and regulatory balance innate immune responses in liver cells." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677270.

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Birnhuber, A., S. Crnkovic, L. M. Marsh, V. Biasin, J. Wilhelm, W. Graninger, A. Olschewski, H. Olschewski, and G. Kwapiszewska. "Exacerbated Lung Function and Eosinophilic Inflammation After Blockage of Innate Immune Signalling in a Mouse Model of Systemic Sclerosis-Associated Lung Fibrosis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3078.

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Cipriani, Barbara, Alan Naylor, Gavin Milne, Barbara Young, Rupert Satchell, Sourav Sarkar, Zoe Smith, et al. "Abstract 1631: GPR65 is a critical mediator of low pH induced immunosuppressive signalling in tumor associated macrophages: Human target validation of GPR65 as a novel innate immune checkpoint and discovery of potent, selective GPR65 antagonists." 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.am2021-1631.

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