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Author:
Publisher:
ISBN: 9789461697240
Category :
Languages : en
Pages : 272
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Book Description
Author:
Publisher:
ISBN: 9789461697240
Category :
Languages : en
Pages : 272
Get Book Here
Book Description
Author: Abdulraouf Ramadan
Publisher: Frontiers Media SA
ISBN: 2889452840
Category : Diseases
Languages : en
Pages : 207
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Book Description
The immune system detects "danger" through a series of what we call pathogen-associated molecular patterns (PAMPs) or damage-associated molecular pattern molecules (DAMPs), working in concert with both positive and negative signals derived from other tissues. PAMPs are molecules associated with groups of pathogens that are small molecular motifs conserved within a class of microbes. They are recognized by Toll-like receptors (TLRs) and other pattern recognition receptors. A vast array of different types of molecules can serve as PAMPs, including glycans and glycoconjugates. Bacterial lipopolysaccharides (LPSs), endotoxins found on the cell membranes of Gram-negative bacteria, are considered to be the prototypical class of PAMPs. LPSs are specifically recognized by TLR4, a recognition receptor of the innate immune system. Other PAMPs include bacterial flagellin (recognized by TLR5), lipoteichoic acid from Gram-positive bacteria, peptidoglycan, and nucleic acid variants normally associated with viruses, such as double-stranded RNA, recognized by TLR3 or unmethylated CpG motifs, recognized by TLR9. DAMPs, also known as alarmins, are molecules released by stressed cells undergoing necrosis that act as endogenous danger signals to promote and exacerbate the immune and inflammatory response. DAMPs vary greatly depending on the type of cell (epithelial, mesenchymal, etc.) and injured tissue. Some endogenous danger signals include heat-shock proteins, HMGB1 (high-mobility group box 1), reactive oxygen intermediates, extracellular matrix breakdown products such as hyaluronan fragments, neuromediators, and cytokines like the interferons (IFNs). Non-protein DAMPs include ATP, uric acid, heparin sulfate, and DNA. Furthermore, accumulating evidence supports correlation between alarmins and changes in the microbiome. Increased serum or plasma levels of these DAMPs have been associated with many inflammatory diseases, including gastric and intestinal inflammatory diseases, graft-versus-host disease (GVHD), sepsis and multiple organ failure, allergies particularly in the lungs, atherosclerosis, age-associated insulin resistance, arthritis, lupus, neuro-inflammation/degeneration and more recently in tumors, which is particularly interesting with the emergence of immunotherapies. Therapeutic strategies are being developed to modulate the expression of these DAMPs for the treatment of these diseases. A vast number of reviews have already been published in this area; thus, in an effort to not duplicate what has already been written, we will focus on recent discoveries particularly in disease models that are epidemic in Western society: intestinal chronic inflammatory diseases including GVHD and its relationship with the microbiome, chronic infectious diseases, allergies, autoimmune diseases, neuroinflammation and cancers. We will also focus on the basic cellular roles of macrophages, T cells and B cells. This research topic brings together sixteen articles that provide novel insights into the mechanisms of action of DAMPS/alarmins and their regulation and subsequent immunologically driven responses.
Author: Massimo Amadori
Publisher: Academic Press
ISBN: 0128019743
Category : Medical
Languages : en
Pages : 278
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Book Description
The Innate Immune Response to Non-infectious Stressors: Human and Animal Models highlights fundamental mechanisms of stress response and important findings on how the immune system is affected, and in turn affects such a response. In addition, this book covers the crucial link between stress response and energy metabolism, prompts a re-appraisal of some crucial issues, and helps to define research priorities in this fascinating, somehow elusive field of investigation. Provides insights into the fundamental homeostatic processes vis-à-vis stressors to help in investigation Illustrates the depicted tenets and how to offset them against established models of response to physical and psychotic stressors in both animals and humans Covers the crucial issue of the immune response to endocrine disruptors Includes immunological parameters as reporter system of environmental adaptation Provides many illustrative examples to foster reader understanding
Author: Shie-Liang Hsieh
Publisher: Springer Nature
ISBN: 9811515808
Category : Medical
Languages : en
Pages : 240
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Book Description
This book systemically presents the latest research on lectins, covering all the major topics in the field, including the heterocomplex of lectins and Toll-like receptors, protective versus pathogenic functions in connection with microbial infections, and novel strategies for enhancing host immunity against infectious diseases caused by viruses, bacteria, and fungi. Lectins are a large group of glycan-binding proteins that recognize diverse glycan and non-glycan structures expressed on prokaryotic and eukaryotic cells, and are vital to cell-cell interactions, the attachment of microbes to host cells, and the recognition and activation of immune responses to exogenous and endogenous danger signals. The composition and structure of microbes are complex and include numerous ‘pathogen-associated molecular patterns’ or ‘damage-associated molecular patterns’. As such, microbes’ interactions with immune cells activate multiple innate immunity receptors and produce distinct inflammatory reactions, which can be protective to contain microbial invasion, or pathogenic to cause tissue damage and shock syndrome in the host. The book shares lessons learned from state-of-the art research in this field, highlights the latest discoveries, and provides insightful discussions on lectin-mediated inflammatory reactions, while also outlining future research directions.
Author: Kenneth Murphy
Publisher: Garland Science
ISBN: 9780815344575
Category : Medical
Languages : en
Pages :
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Book Description
The Janeway's Immunobiology CD-ROM, Immunobiology Interactive, is included with each book, and can be purchased separately. It contains animations and videos with voiceover narration, as well as the figures from the text for presentation purposes.
Author: Philip Conaghan
Publisher: Oxford University Press
ISBN: 0199642486
Category : Medical
Languages : en
Pages : 1553
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Book Description
A strong clinical emphasis is present throughout this volume from the first section of commonly presenting problems through to the section addressing problems shared with a range of other clinical sub-specialties.
Author: Cheston B. Cunha
Publisher: Oxford University Press
ISBN: 0190888369
Category : Medical
Languages : en
Pages : 1521
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Book Description
Preceded by Clinical infectious disease / [edited by] David Schlossberg. Second edtion. 2015.
Author: Paul Matthew Gallo
Publisher:
ISBN:
Category :
Languages : en
Pages : 150
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Book Description
Systemic lupus erythematosus (SLE) is complex autoimmune disease in which autoantibodies form against double stranded DNA (dsDNA) and nuclear antigens. Autoantigen immune complexes form, deposit in the vasculature, and cause multisystem organ damage. Both genetic and environmental factors contribute to the development of SLE. This thesis will explore three major themes found in the study of SLE: 1) Bacterial infection as an environmental trigger, 2) cytokine dysregulation in immune cells, and 3) the treatment of end organ damage in the form of lupus nephritis. Viral infections have long been associated with the development of systemic autoimmune disease, but the mechanisms by which chronic bacterial infections may promote autoimmunity remain unclear. In chapter three we show that a component of bacterial biofilms, the amyloid-like protein "curli", irreversibly forms fibers with bacterial or eukaryotic DNA during biofilm formation. This interaction accelerates amyloid polymerization and creates potent immunogenic complexes that activate immune cells, including dendritic cells, to produce cytokines such as type I interferons, which are pathogenic in SLE. When given systemically, curli/DNA composites trigger immune activation and production of autoantibodies in lupus-prone and wild type mice. We also found that infection with curli-producing bacteria triggered higher autoantibody titers in lupus-prone mice compared to curli-deficient bacteria. These data provide a mechanism by which the microbiome and biofilm-producing enteric infections may contribute to the progression of SLE and point to a potential molecular target for treatment of autoimmunity. Cytokine dysregulation is also common in SLE patients. Serum cytokines are often elevated during active disease, including type I IFNs and IL-10. In chapter four we demonstrate that Il10 is a type I IFN response gene and has increased basal expression in dendritic cells (DCs) derived from pre-disease lupus-prone Sle1,2,3 mice. We show that Sle1,2,3-derived DCs overproduce IL-10 in response to TLR ligands and that this is the result of autocrine signaling though the type I IFN receptor (IFNAR). These results suggest that dysregulation of cytokine signaling in the myeloid compartment may contribute to IL-10 dysregulation in SLE. Renal disease remains a major cause of morbidity and mortality in SLE. A number of mouse models of chronic kidney disease have implicated the EGFR-family receptors in the progression of renal fibrosis and dysfunction. In chapter five we show that renal expression of ErbB2 is increased in murine lupus. We therefore asked if EGFR-family inhibition could prevent murine lupus nephritis. To test this possibility we used lapatinib, an EGFR-ErbB2 dual kinase inhibitor, in an IFN-accelerated model of murine lupus. We found that lapatinib administration lowered autoantibody levels but worsened renal disease. Lapatinib failure to treat murine lupus nephritis despite lowered autoantibody levels suggests EGFR-family signaling is required for tissue repair in the acute phase of kidney injury. Together this thesis clearly demonstrates the complexity of systemic autoimmune disease - bringing us to the crossroads of immunity and tolerance. The combination of both environmental triggers (e.g. bacterial infection) and genetic susceptibility (e.g. intrinsic cytokine dysregulation) leads to end organ damage (e.g. lupus nephritis). Here we sought to explore each aspect of disease progression in the hopes to develop better interventions for systemic autoimmune disease.
Author: Adriano Rossi
Publisher: Springer Science & Business Media
ISBN: 376437506X
Category : Medical
Languages : en
Pages : 246
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Book Description
This book provides readers with an up-to-date and comprehensive view on the resolution of inflammation and on new developments in this area, including pro-resolution mediators, apoptosis, macrophage clearance of apoptotic cells, possible novel drug developments.
Author: Lesley A. Doughty
Publisher: Springer Science & Business Media
ISBN: 1461502454
Category : Medical
Languages : en
Pages : 296
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Book Description
This unique volume provides a mechanistic look at key aspects of the inflammatory response seen in critical illness. Key cells and mediators involved in the innate inflammatory response and the pathways employed to combat infection or respond to injury are emphasized. It has become clear that a delicate balance exists to allow eradication of infection with minimal immune-mediated tissue injury in the process. For this reason an up-to-date discussion of how the inflammatory response down regulates itself has been included. The inflammatory response in the critically ill is vastly different than in healthy hosts. For this reason, discussions about the mechanisms of pharmacologic immune suppression and other less commonly considered immunomodulated states seen frequently in critical care medicine have been included. Given the differences in immune function seen in critical illness, the importance of considering the immune system an organ whose function must be monitored and optimized for the best possible outcome has been highlighted. In addition, we have included up-to-date discussions of prevention and diagnostic approaches to extremely common infectious entities which must be monitored for and treated appropriately in the setting of critical illness induced immune dysfunction.
