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Dans les sociétés occidentales et dans les régions du monde à forte croissance économique, les maladies allergiques se développent selon une progression épidémique. Ce livre explique comment on en est arrivé là. Quelles sont les causes de l'épidémie d'allergies ? Plusieurs hypothèses ont été avancées. Les progrès de l'hygiène et la disparition des parasitoses intestinales à la fin de la première moitié du XXe siècle ont assurément joué un rôle significatif. En effet, la cohabitation avec les microbes et parasites de toutes sortes entretenait une stimulation immunitaire constante qui semble nous avoir protégés contre les dérèglements de notre immunité. Les transformations de l'habitat et les nouveaux modes alimentaires ont très probablement participé à l'émergence de nouvelles maladies allergiques, mais aussi de maladies auto-immunes telles que la sclérose en plaques ou la polyarthrite rhumatoïde. En revanche, la pollution atmosphérique ne semble pas impliquée dans l'explosion des maladies allergiques; elle peut toutefois jouer un rôle dans leurs exacerbations. Finalement, les allergies sont peut-être le prix à payer pour notre civilisation de bien-être et de longévité… Quels sont les traitements contre les allergies ? Sur la base de ce que l'on connaît aujourd'hui des mécanismes de l'allergie, l'auteur explique quels sont les moyens de diagnostic fiables et les stratégies de traitement rendues possibles par la biologie moderne. Il développe les traitements actuels des différentes formes d'allergie, notamment les approches telles que l'immunothérapie et les nouvelles biothérapies. Il aborde également les médecines parallèles et souligne l'importance de l'effet placebo dans les traitements.

Immunologic diseases.

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The cytoplasm of Gram-negative bacteria is bound by three layers: an inner membrane, a layer of peptidoglycan, and an outer membrane. The outer membrane is an asymmetric lipidic bilayer, with phospholipids on its inner surface and lipopolysaccharides (LPSs) on the outside, with the latter being the major component of the outer leaflet and covering nearly three-quarters of the total outer cell surface. All LPSs possess the same general chemical architecture independently of bacterial activity (pathogenic, symbiotic, commensal), ecological niche (human, animal, soil, plant, water), or growth conditions. Endotoxins are large amphiphilic molecules consisting of a hydrophilic polysaccharide component and a covalently bound hydrophobic and highly conserved lipid component, termed lipid A (the endotoxin subunit). The polysaccharide component can be divided into two subdomains: the internal and conserved core region as well as the more external and highly variable O-specific chain, also referred to as the O-antigen due to its immunogenic properties. LPSs are endotoxins, one of the most potent class of activators of the mammalian immune system; they can be released from cell surfaces of bacteria during multiplication, lysis, and death. LPS can act through its biological center (lipid A component) on various cell types, of which macrophages and monocytes are the most important.

Immunologic diseases.

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Immunologic diseases.

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Lipids are best known as energy storing molecules and core-components of cellular membranes, but can also act as mediators of cellular signaling. This is most prominently illustrated by the paramount importance of the phospholipase C (PLC) and phosphoinositide 3-kinase (PI3K) signaling pathways in many cells, including T cells and cancer cells. Both of these enzymes use the lipid phosphatidylinositol(4,5)bisphosphate (PIP2) as their substrate. PLCs produce the lipid product diacylglycerol (DAG) and soluble inositol(1,4,5)trisphosphate (IP3). DAG acts as a membrane tether for protein kinase C and RasGRP proteins. IP3 is released into the cytosol and controls calcium release from internal stores. The PI3K lipid product phosphatidylinositol(3,4,5)trisphosphate (PIP3) controls signaling by binding and recruiting effector proteins such as Akt and Itk to cellular membranes. Recent research has unveiled important signaling roles for many additional phosphoinositides and other lipids. The articles in this volume highlight how multiple different lipids govern T cell development and function through diverse mechanisms and effectors. In T cells, lipids can orchestrate signaling by organizing membrane topology in rafts or microdomains, direct protein function through covalent lipid-modification or non-covalent lipid binding, act as intracellular or extracellular messenger molecules, or govern T cell function at the level of metabolic regulation. The cellular activity of certain lipid messengers is moreover controlled by soluble counterparts, exemplified by symmetric PIP3/inositol(1,3,4,5)tetrakisphosphate (IP4) signaling in developing T cells. Not surprisingly, lipid producing and metabolizing enzymes have gained attention as potential therapeutic targets for immune disorders, leukemias and lymphomas.

Immunologic diseases.

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The cytoplasm of Gram-negative bacteria is bound by three layers: an inner membrane, a layer of peptidoglycan, and an outer membrane. The outer membrane is an asymmetric lipidic bilayer, with phospholipids on its inner surface and lipopolysaccharides (LPSs) on the outside, with the latter being the major component of the outer leaflet and covering nearly three-quarters of the total outer cell surface. All LPSs possess the same general chemical architecture independently of bacterial activity (pathogenic, symbiotic, commensal), ecological niche (human, animal, soil, plant, water), or growth conditions. Endotoxins are large amphiphilic molecules consisting of a hydrophilic polysaccharide component and a covalently bound hydrophobic and highly conserved lipid component, termed lipid A (the endotoxin subunit). The polysaccharide component can be divided into two subdomains: the internal and conserved core region as well as the more external and highly variable O-specific chain, also referred to as the O-antigen due to its immunogenic properties. LPSs are endotoxins, one of the most potent class of activators of the mammalian immune system; they can be released from cell surfaces of bacteria during multiplication, lysis, and death. LPS can act through its biological center (lipid A component) on various cell types, of which macrophages and monocytes are the most important.

Immunologic diseases.