Gotowe bibliografie tematyczne / Immune signalling

Gotowa bibliografia na temat „Immune signalling”

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Data publikacji: 25 maja 2024

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Artykuły w czasopismach na temat "Immune signalling"

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Hegde, Sushmitha, Amarendranath Soory, Bhagyashree Kaduskar i Girish S. Ratnaparkhi. "SUMO conjugation regulates immune signalling". Fly 14, nr 1-4 (31.08.2020): 62–79. http://dx.doi.org/10.1080/19336934.2020.1808402.

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GOODRIDGE, H. S., i M. M. HARNETT. "Introduction to immune cell signalling". Parasitology 130, S1 (marzec 2005): S3—S9. http://dx.doi.org/10.1017/s0031182005008115.

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The dynamic interaction of cells of the immune system with other cells, antigens and secreted factors determines the nature of an immune response. The response of individual cells is governed by the sequence of intracellular signalling events triggered following the association of cell surface molecules during cell-cell contact or the detection of soluble molecules of host or pathogen origin. In this review we will first outline the general principles of intracellular signal transduction. We will then describe the signalling pathways triggered following the recognition of antigen, as well as the detection of cytokines, and discuss how the signalling pathways activated regulate the effector response.
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Kumar, Santosh, i Shweta Jain. "Immune signalling by supramolecular assemblies". Immunology 155, nr 4 (24.09.2018): 435–45. http://dx.doi.org/10.1111/imm.12995.

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Pittman, Quentin J., i Abdeslam Mouihate. "Immune Signalling to the Brain". Journal of Physiology 550, nr 1 (lipiec 2003): 1. http://dx.doi.org/10.1113/jphysiol.2003.045609.

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Burnstock, Geoffrey, i Jean-Marie Boeynaems. "Purinergic signalling and immune cells". Purinergic Signalling 10, nr 4 (29.10.2014): 529–64. http://dx.doi.org/10.1007/s11302-014-9427-2.

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Dragoni, Silvia, i Patric Turowski. "Vascular Signalling". Cells 12, nr 16 (10.08.2023): 2038. http://dx.doi.org/10.3390/cells12162038.

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Maurya, Rashmi, Deepti Srivastava, Munna Singh i Samir V. Sawant. "Envisioning the immune interactome in Arabidopsis". Functional Plant Biology 47, nr 6 (2020): 486. http://dx.doi.org/10.1071/fp19188.

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During plant–pathogen interaction, immune targets were regulated by protein–protein interaction events such as ligand-receptor/co-receptor, kinase-substrate, protein sequestration, activation or repression via post-translational modification and homo/oligo/hetro-dimerisation of proteins. A judicious use of molecular machinery requires coordinated protein interaction among defence components. Immune signalling in Arabidopsis can be broadly represented in successive or simultaneous steps; pathogen recognition at cell surface, Ca2+ and reactive oxygen species signalling, MAPK signalling, post-translational modification, transcriptional regulation and phyto-hormone signalling. Proteome wide interaction studies have shown the existence of interaction hubs associated with physiological function. So far, a number of protein interaction events regulating immune targets have been identified, but their understanding in an interactome view is lacking. We focussed specifically on the integration of protein interaction signalling in context to plant–pathogenesis and identified the key targets. The present review focuses towards a comprehensive view of the plant immune interactome including signal perception, progression, integration and physiological response during plant pathogen interaction.
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Kee, Tay Hwee, Patricia Vit i Alirio J. Melendez. "Sphingosine kinase signalling in immune cells". Clinical and Experimental Pharmacology and Physiology 32, nr 3 (marzec 2005): 153–61. http://dx.doi.org/10.1111/j.1440-1681.2005.04166.x.

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Barragan, A., J. M. Weidner, Z. Jin, E. R. Korpi i B. Birnir. "GABAergic signalling in the immune system". Acta Physiologica 213, nr 4 (1.03.2015): 819–27. http://dx.doi.org/10.1111/apha.12467.

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Fiil, Berthe K., i Mads Gyrd‐Hansen. "Met1‐linked ubiquitination in immune signalling". FEBS Journal 281, nr 19 (12.08.2014): 4337–50. http://dx.doi.org/10.1111/febs.12944.

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Rozprawy doktorskie na temat "Immune signalling"

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Moon, Alice E. "Immune signalling in insect cells". Thesis, Kingston University, 2009. http://eprints.kingston.ac.uk/20407/.

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Immune responses in insects include components and mechanisms that are highly evolutionarily conserved. In addition to providing insight into the insects themselves, knowledge of the conserved mechanisms involved in insect immunity can offer valuable insight that is broadly relevant to a wide variety of other species. Three aspects of insect immune cell signalling have been studied here. Cell signalling responses have been investigated in two insect cell lines following treatment with double stranded (ds) RNA, a common intermediate of viral replication. It has been established that both cell lines investigated, from the fruitfly Drosophila melanogaster and vector mosquito Aedes albopictus, do not exhibit activation of mitogen activated protein kinases (MAPKs) or NF-KB proteins as a direct response to dsRNA. Secondly, a detailed analysis of the mechanisms of transcriptional regulation has been carried out on the Drosophila drosomycin gene, a key factor both in terms of its function during the immune response and in terms of its role during previous characterisation of Drosophila immune signalling. The drosomycin promoter was found to be regulated independently by the Toll and IMD signalling pathways via distinct sequence elements. Finally, investigation of the responses of an A. albopictus cell line to treatment with bacterial cell wall components has revealed key differences in the mechanisms involved in immune-induced regulation of transcription compared with the model established in Drosophila. A role for p38 MAPK has been identified in the negative regulation of transcription of A. albopictus cecropin Ai, an inducible antimicrobial peptide gene.
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Ng, Siaw Wei. "Calcium signalling in immune cells". Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:b3843e43-9503-4855-a280-35c0d28f65e6.

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Inappropriate stimulation of mast cells can trigger allergies including asthma, allergic rhinitis and eczema which, combined, affect almost 30% of the population in western societies. Mast cell activation begins with aggregation of IgE receptors in response to antigen. This then triggers a series of reactions resulting in the tyrosine phosphorylation of Syk kinase, PKC activation and ultimately both degranulation and secretion of leukotrienes and cytokines. CRAC channels are expressed on mast cells, and are essential for IgE-mediated mast cell activation. Previous work in our laboratory has shown that local Ca2+ influx through CRAC channels activates Ca2+-dependent phopholipase A₂, ERK and 5-lipoxygenase, resulting in LTC₄ secretion from mast cells. Therefore, I have investigated how Ca2+ microdomains through CRAC channels are detected and how they trigger cellular responses. I find that phosphorylation of Syk following antigen stimulation is enhanced by Ca2+ influx through CRAC channels. I also show synergy between CRAC channels and antigen in activating Syk. These findings reveal a novel positive feedback step in mast cell activation, where local Ca2+ entry through CRAC channels activates Syk which, in turn, supports CRAC channels. Earlier work from our group has demonstrated that in RBL cells, Ca2+ influx through CRAC channels induces expression of the gene c-fos, an important regulator of pro-inflammatory gene expression. I have discovered that local Ca2+ entry is sensed by the non-receptor tyrosine kinase Syk, which accumulates at the cell periphery. Syk then signals to the nucleus through recruitment of the transcription factor STAT5. The results therefore identify Syk as a new link in excitation-transcription coupling, converting local Ca2+ influx into expression of genes that are essential for immune cell activation. Activation of G protein-coupled cysteinyl leukotriene type I receptors by the pro-inflammatory molecule LTC₄ is tightly linked to immune cell function and the receptor is an established therapeutic target for allergies including asthma. Desensitization of cysteinyl leukotriene type I receptors arises following protein kinase C-dependent phosphorylation of three serine residues in the receptor C-terminus. Here I show that abolishing leukotriene receptor desensitization suppresses agonist-driven gene expression. Physiological concentrations of LTC₄ led to repetitive cytoplasmic Ca2+ oscillations, which were accompanied by the opening of store-operated CRAC channels in the plasma membrane. Ca2+ microdomains near the open channels were relayed to the nucleus to increase expression of the transcription factor c-fos. In the absence of receptor desensitization, agonist-driven gene expression was suppressed. Mechanistically, stimulation of non-desensitizing receptors evoked prolonged Ca2+ release, which led to accelerated Ca2+-dependent inactivation of CRAC channels and a subsequent loss of excitation-transcription coupling. Rather than serving to turn off a biological response, the experiments show that reversible receptor desensitization is an ‘on’switch’, sustaining long-term signalling in the immune system.
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Hamer, Rebecca K. "The structural basis of immune receptor signalling". Thesis, University of Oxford, 2008. http://ora.ox.ac.uk/objects/uuid:32312040-2e22-4fe3-b05e-6f868233e27e.

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This work investigates the mechanisms of binding of T cell receptors (TCRs) to Class I MHC-peptide complexes (pMHC). The structure of a TCR specific for the Melan-A tumour antigen bound to its cognate pMHC was solved to a resolution of 2.5 Å which gives insight into how this TCR could be mutated to optimize binding and subsequently used as a cancer vaccine. Detailed sequence and geometric analyses of all currently available structures of Class I TCR-pMHC complexes revealed that TCRs can bind to pMHC with a range of orientations, yet always focus on the central portion of the peptide and use a specific subset of six residues on the MHC helices for binding. The most striking finding was the use of aromatic residues in the TCR CDR loops to bind to residue Q155 on the MHC α2 helix. Attempts were also made to express and purify Toll-like receptors (TLRs) with the aim of solving one or more of these structures. However, despite testing of over 50 different constructs from 12 different TLRs or associated proteins, insufficient soluble protein expression was obtained for crystallization trials. Finally, a protein disorder prediction tool was developed to aid construct design for structural biology studies and improve the chances of obtaining protein crystals. This tool is based on a novel type of neural network and blind tests comparing it to 8 other disorder prediction tools showed it is one of the best in the field. It is freely available at www.strubi.ox.ac.uk/RONN. Analysis of large datasets revealed that the position of order/disorder transitions is quite precisely defined in amino-acid sequences and that transition regions have an amino acid composition distinct from that of bulk ordered and disordered sequences. There is a steady decrease in order-promoting residues on the ordered side of boundaries as well as a weak sequence signal, both of which signify the approaching disorder and may prove useful for improving existing disorder prediction tools.
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Akha, Amir Akbar Sadighi. "Signalling through the B lymphocyte antigen receptor". Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318620.

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Morris-Davies, A. C. "Functional analysis of poly-ubiquitin chains in immune signalling". Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1383788/.

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NF-κB transcription factors play essential roles in regulating the expression of a large array of genes involved in immune and inflammatory responses, cell proliferation, apoptosis and oncogenesis. In recent years, ubiquitination of key components has emerged as a crucial regulatory mechanism in NF-κB signalling pathways. This can either directly modulate the activity of the target substrate or provide a scaffold for the recognition and recruitment of other signalling molecules via their respective ubiquitin binding domains. NEMO, the regulatory subunit of the IKK complex, is a prime example of a signalling component which interacts with ubiquitin chains of different topologies as well as being modified by ubiquitination. These events are thought to regulate the activation of the kinase subunits of the complex, IKKα and IKKβ, which ultimately results in liberation of NF-κB and translocation to the nucleus. NEMO itself possesses two ubiquitin-binding domains: the CoZi/UBAN domain and a C-terminal zinc finger (ZF). The work presented in this thesis shows that the synergistic action of these two domains confers specificity for K63-linked ubiquitin chains. Importantly, chain length plays a crucial role in these binding events. The discovery that NEMO becomes modified by the E3 ligase LUBAC with a novel type of ubiquitin chain, termed linear, opened up a whole new exciting area of research. So far, LUBAC is the only E3 ligase known to synthesize this type of chain. This thesis provides a first glimpse into the mechanistic determinants which allow LUBAC to enforce the formation of linear ubiquitin chains and demonstrates, for the first time, that one of its subunits, HOIL-1L, transfers ubiquitin to a substrate via a thioester intermediate.
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Dawson, Charlotte Helen. "STAT 6 and IL-4 signalling". Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245716.

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Silva, Couto Daniel. "Regulation of receptor kinase-mediated immune signalling by dynamic phosphorylation". Thesis, University of East Anglia, 2015. https://ueaeprints.uea.ac.uk/59391/.

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Plants recognize pathogen-associated molecular patterns (PAMPs) via cell surface-localized pattern recognition receptors (PRRs), initiating a broad-spectrum defense response against pathogens, known as PRR-triggered immunity (PTI). However, immunity comes at a cost; and immune responses need to be tightly regulated. How PTI signalling is negatively regulated in plants is not fully understood. PRRs are present at the plasma membrane in dynamic kinase complexes that heavily rely on trans-phosphorylation to initiate signaling. The Arabidopsis cytoplasmic kinase BIK1 associates with different PRRs and plays a central role in the activation of downstream immune signaling. In this study, we identify the protein phosphatase PP2C38 as a negative regulator of BIK1 activity and BIK1-mediated immunity. PP2C38 dynamically associates with BIK1, as well as with the PRRs FLS2 and EFR, but not with the regulatory receptor kinase (RK) BAK1. PP2C38 regulates PAMP-induced BIK1 phosphorylation and impairs the phosphorylation of the NADPH oxidase RBOHD by BIK1, leading to reduced oxidative burst and stomatal immunity. Notably, upon PAMP perception, PP2C38 is phosphorylated on serine 77, most likely by BIK1, and dissociates from the PRR-BIK1 complex. We suggest that this mechanism relieves the negative regulation imposed by PP2C38 to enable efficient BIK1 activation. This study uncovers an important regulatory mechanism of this central immune component, and extends our knowledge on how plant immunity is appropriately controlled.
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Wahl, Karen. "Role of Notch signalling in the induction of immune responses". Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/23239.

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The expression and the role of Notch receptors and ligands during the induction of an immune response were investigated. I have shown that components of the Notch pathway were present in peripheral CD4 and CD8 T cells. Upon culturing and activation in vitro, in many Notch components were differentially expressed, in particular targets of Notch activation. In contrast, bone marrow-derived dendritic cells (DCs) expressed only low levels of Notch targets. However, the Notch ligand Jagged1 was strongly upregulated upon maturation of DCs with TNFα or LPS. By regulating the expression of the ligands, a role for antigen presenting cells (APCs) as the “signalling cells” is likely, whereas T cells expressing Notch receptors and Notch target genes may be the “receiving cells”. To investigate this hypothesis in vivo, transgenic mice with inducible overexpression of Jagged1 or Delta1 in DCs were generated. An in vitro approach to study the role of Notch ligands on APCs was carried out using an I-Ab transfected murine fibroblast cell line (I-Ab+ L cells) with endogenous B7.1 expression. I-Ab+ L cells co-transfected with Jagged1 or Delta (Jagged1+ or Delta1+L cells, respectively) were used as APCs in a mixed lymphocyte reaction (MLR) in vitro. Jagged1+ and I-Ab+ L cells induced similar levels of allogeneic T cell proliferation, whereas Delta1+ L cells had a slightly increased capacity to activate T cell proliferation. There were no phenotypical differences or changes in the level of apoptosis observed between T cells activated by Jagged1+, Delta1+ or I-Ab+ L cells. However, IFNγ secretion by T cells in response to Jagged1+ L cells was strongly reduced, whereas Delta1+ and I-Ab+ L cells induced normal levels of IFNγ secretion. There were no significant differences neither in the level of intracellular IFNγ nor of IFNγ transcripts between T cells in response to Jagged1+, Delta1+ or I-Ab+ L cells. Therefore I hypothesise that Jagged1-induced Notch signalling may be involved at the level of IFNγ secretion.
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Beyers, Albertus Daniel. "Transmembrane signalling by the CD2 and CD4 molecules of T lymphocytes". Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.291324.

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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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Książki na temat "Immune signalling"

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Verma, Navin Kumar, Dermot Kelleher i Thai Tran, red. Adaptor Protein Regulation in Immune Signalling. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-703-4.

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(Editor), William Harnett, i Les Chappell (Editor), red. Subversion of Immune Cell Signalling by Parasites. Cambridge University Press, 2006.

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Fleischmann, Roy. Signalling pathway inhibitors. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0081.

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Oral, small-molecule signalling pathway inhibitors, including ones that inhibit the JAK and SyK pathways, are currently in development for the treatment of rheumatoid arthritis (RA). Tofacitinib is an orally administered small-molecule inhibitor that targets the intracellular Janus kinase 3 and 1 (JAK1/3) molecules to a greater extent than JAK2 while baricitinib (formerly INCB028050) predominantly inhibits JAK1/2. Many of the proinflammatory cytokines implicated in the pathogenesis of RA utilize cell signalling that involves the JAK-STAT pathways and therefore inhibition of JAK-STAT signalling, by targeting multiple RA-associated cytokine pathways, has the potential to simultaneously reduce inflammation, cellular activation, and proliferation of key immune cells. Fostamatinib disodium is an orally available inhibitor of spleen tyrosine kinase (SyK), which is a cytoplasmic tyrosine kinase that is an important mediator of immunoreceptor signalling in mast cells, macrophages, neutrophils, and B cells. Interruption of SyK signalling may interrupt production of tumour necrosis factor (TNF) and metalloproteinase and therefore affect RA disease activity. Tofacitinib has been investigated in multiple phase 2 and phase 3 trials which have investigated its efficacy (clinical, functional, and radiographic) and safety in patients who have failed disease-modifying anti-inflammatory drugs (DMARDs) as monotherapy or in combination with DMARDs, compared to an inhibitor of tumour necrosis factor alpha (TNFα‎) and in patients who have failed TNFα‎ inhibitors. The efficacy of fostamatinib and baricitinib has been investigated in phase 2 trials; both are in large phase 3 clinical programmes. Each of these medications has demonstrated efficacy; their safety profile has been shown to be different from each other and from currently approved biological agents. This chapter discusses what is currently known and understood about their efficacy and safety.
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Abracchio, Maria P., i Michael Williams. Purinergic and Pyrimidinergic Signalling II: Cardiovascular, Respiratory, Immune, Metabolic and Gastrointestinal Tract Function. Springer, 2014.

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Abracchio, Maria P., i Michael Williams. Purinergic and Pyrimidinergic Signalling II: Cardiovascular, Respiratory, Immune, Metabolic and Gastrointestinal Tract Function. Springer Berlin / Heidelberg, 2012.

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Abracchio, Maria P., i Michael Williams. Purinergic and Pyrimidinergic Signalling II: Cardiovascular, Respiratory, Immune, Metabolic and Gastrointestinal Tract Function. Springer London, Limited, 2012.

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Geri, Guillaume, i 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, i 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 i 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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Części książek na temat "Immune signalling"

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Wardle, E. Nigel. "Signalling in Immune Reactions". W Guide to Signal Pathways in Immune Cells, 201–46. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-538-5_12.

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Wardle, E. Nigel. "Introduction to Signalling Cascades". W Guide to Signal Pathways in Immune Cells, 37–75. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-538-5_4.

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Carlin, Leo M., Konstantina Makrogianneli, Melanie Keppler, Gilbert O. Fruhwirth i Tony Ng. "Visualisation of Signalling in Immune Cells". W Methods in Molecular Biology, 97–113. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-461-6_7.

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Dubyak, G. R. "Role of P2 Receptors in the Immune System". W Purinergic and Pyrimidinergic Signalling II, 323–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56921-0_10.

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Dallman, Margaret J., Brian Champion i Jonathan R. Lamb. "Notch Signalling in the Peripheral Immune System". W Novartis Foundation Symposia, 268–78. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470871628.ch20.

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Virgilio, F. Di, V. Vishwanath i D. Ferrari. "On the Role of the P2X7 Receptor in the Immune System". W Purinergic and Pyrimidinergic Signalling II, 355–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56921-0_11.

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Fitzpatrick, Julie L. "Induction of Immune Responses in the Bovine Mammary Gland". W Intercellular Signalling in the Mammary Gland, 271–72. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1973-7_51.

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Mulhern, Orla, Barry Harrington i Andrew G. Bowie. "Modulation of Innate Immune Signalling Pathways by Viral Proteins". W 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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Guzella, Thiago, Tomaz Mota-Santos, Joaquim Uchôa i Walmir Caminhas. "Modelling the Control of an Immune Response Through Cytokine Signalling". W Lecture Notes in Computer Science, 9–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/11823940_2.

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Galvão, Izabela, Lirlândia P. Sousa, Mauro M. Teixeira i Vanessa Pinho. "PI3K Isoforms in Cell Signalling and Innate Immune Cell Responses". W 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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Streszczenia konferencji na temat "Immune signalling"

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

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Suprun, E., E. Nagovitsina, O. Lebedko i S. Suprun. "Genes Polymorphisms of Signalling Molecules of the Immune System as a Factor of Uncontrolled Bronchial Asthma". W 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.a3054.

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O'Malley, Grace, Kevin Lynch, Serika Naicker, Paul Lohan, Athina Rigalou, Thomas Ritter, Laurence J. Egan i Aideen E. Ryan. "Abstract 2693: Inflammatory signalling in the colon tumour microenvironment enhances stromal cell mediated suppression of anti-tumour immune responses". W 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.am2017-2693.

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Kandolf Sekulović, Lidija. "TOXICITIES OF TARGETED THERAPY AND IMMUNE-RELATED ADVERSE DRUG REACTIONS OF IMMUNOTHERAPY IN THE TREATMENT OF METASTATIC MELANOMA". W Okrugli sto s međunarodnim učešćem "Melanom". Akademija nauka i umjetnosti Bosne i Hercegovine, 2018. http://dx.doi.org/10.5644/pi2019.180.04.

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Targeted therapy and immunotherapy changed the treatment landscape for metastatic melanoma, which is chemotherapy resistant cancer. In pre-innovation era, the overall survival of patients with metastatic melanoma was 6 months, while today 5-year overall survival rate of 34% (and 50% in good prognostic groups) is evident. However, both treatments have their side effects, and cutaneous are the most frequent. Treating physicians in oncology centres, but also primary care specialists, need to be aware of their spectrum which differs for each class of drug: BRAF inhibitors, MEK inhibitors and immunotherapy with anti-PD1 and anti-CTLA4. While BRAF inhibitors have the most prominent adverse effects which are class specific, there are also drug-specific adverse effects. For example, vemurafenib causes photosensitivity, which is not specific for dabrafenib, while dabrafenib induces pyrexia, that occurs much less frequently with other BRAF inhibitors. Cutaneous rash and cutaneous neoplasms which develop due to paradoxical activation of RAS signalling are described with BRAF inhibitor monotherapy. These side-effects are much less common in combination therapy with BRAF and MEK inhibitor, but MEK inhibitor itself causes characteristic acneiform eruption, and serous retinopathy. Immune related adverse drug reactions are a hallmark of the immune checkpoint inhibitor immunotherapy, which can affect every organ system, and most commonly skin, lungs and gastrointestinal system, with differential frequencies recorded with anti-CTLA4 therapy and anti PD-1 therapy. Skin reactions most frequently include pruritus and eczematous reactions, as well as vitiligo-like hypopigmentation, which is linked Melanom 45 to the better response to treatment. In this review, frequent and rare side effects are presented, as well as the current algorithms for their treatment.
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Luo, X., M. Lu, HA Baba, G. Gerken, H. Wedemeyer i R. Broering. "The Hippo signalling is induced by Toll-like receptor 4 activation and regulatory balance innate immune responses in liver cells". W 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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Orafidiya, Folake A., Catherine Davidson, Richard D. Wilkinson, Steve M. Walker, Laura A. Knight, Paul D. Harkin, Nuala McCabe i Richard D. Kennedy. "Abstract 578: Loss of MED12 predicts for a DNA damage repair deficiency phenotype and activates immune signalling via the STING pathway". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-578.

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"Disentangling the multiphasic nature of intracellular calcium responses induced by fungal signals in Lotus japonicus roots". W IS-MPMI Congress. IS-MPMI, 2023. http://dx.doi.org/10.1094/ismpmi-2023-10.

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The recognition of different microbe-associated molecular patterns triggers in the plant the activation of either an immune response or an accommodation program. In both types of responses, Ca2+ is a crucial intracellular messenger, mediating the early stages of the respective signalling pathways. In this work, we analyzed the cytosolic and nuclear Ca2+ changes activated by a set of chitin-related oligomers in different genetic backgrounds of Lotus japonicus roots by using specifically targeted aequorin-based Ca2+ reporters. By means of pharmacological and genetic approaches, we dissected the plant Ca2+ responses into two separable and temporally distinct components. A complementary approach carried out via a cameleon-based bioassay in Medicago truncatula root organ cultures further supports the occurrence of different temporal phases in the observed Ca2+ transients. While the second phase of the Ca2+ change represents the well-known Ca2+ spiking phenomenon, we show that the occurrence of the rapid first phase, which critically depends on the elicitor concentration, correlates with the activation of plant immunity marker genes. Our data provide clues to a better understanding of the subtle boundaries between symbiotic and immunity responses in plant-fungus interactions.
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Birnhuber, A., S. Crnkovic, L. M. Marsh, V. Biasin, J. Wilhelm, W. Graninger, A. Olschewski, H. Olschewski i G. Kwapiszewska. "Exacerbated Lung Function and Eosinophilic Inflammation After Blockage of Innate Immune Signalling in a Mouse Model of Systemic Sclerosis-Associated Lung Fibrosis". W 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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Mulcahy, Victoria, Jose-Ezequiel Martin, Janeane Hails, Richard Sandford, David Jones, Gideon Hirschfield i George Mells. "O10 TNF signalling associated with high risk compared to low risk disease in primary biliary cholangitis: a transcriptomic analysis of peripheral immune cells". W Abstracts of the British Association for the Study of the Liver Annual Meeting, 19–22 September 2023. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2023. http://dx.doi.org/10.1136/gutjnl-2023-basl.10.

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Glynn, S., P. Garrrido-Cuesta, D. Wink, L. Ridnour, S. Ambs, M. Keane, E. Walsh i G. Callagy. "Abstract P2-05-15: NOS2&COX2 activation of TLR4 & EGFR signalling causes poor outcome in oestrogen receptor-negative breast cancer via pro-survival signals and immune polarisation". W Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p2-05-15.

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