Immunopharmacology of Neutrophils
Paul G. Hellewell, T. J. Williams
Academic Press, 1994 - Medical - 334 pages
About the Series:
The consequences for diseases involving the immune system such as AIDS, and chronic inflammatory diseases such as bronchial asthma, rheumatoid arthritis, and atherosclerosis, now account for a considerable economic burden to governments worldwide. In response there has been an enormous research effort investigating the basic mechanisms underlying such diseases, and a tremendous drive to identify novel therapeutic applications for their prevention and treatment. Though a plethora of immunological studies have been published in recent years, little has been written about the implications of such research for drug development. As a consequence, this area has not gained the prominence of other new fields such as molecular pharmacology or neuropharmacology, and a focal information source for the many pharmacologists interested in diseases of the immune system remains unpublished. The Handbook of Immunopharmacology series provides such a source through the commissioning of a comprehensive collection of volumes on all aspects of immunopharmacology. Editors have been sought after for each volume who are not only active in their respective areas of expertise, but who also have a distinctly pharmacological bias to their research. The series follows three main themes, each represented by volumes on individual component topics. The first covers each of the major cell types and classes of inflammatory mediators ("cells and mediators"). The second covers each of the major organ systems and the diseases involving the immune and inflammatory responses that can affect them ("systems"). The third covers different classes of drugs currently used to treat these diseases as well as those under development ("drugs").
About the Book:
This book addresses the key issues that face neutrophils during their very short but extremely important lives. The discovery that neutrophils have the capacity to phagocytose and kill foreign organisms set the stage for a fascinating research field that continues to stimulate exciting new findings throughout the world. Neutrophils target the sites of infection or injury, and are thus equipped with sensors for soluble signals ("chemoattractants") generated in the tissue in response to tissue infection or injury, and sensors for molecules on surfaces. These receptors are important so that the cell can distinguish, for example, activated endothelium to stimulate adherence and emigration, or alternatively the bacterial surface to stimulate phagocytosis and killing. A deficiency in any of these mechanisms can result in life-threatening infection. An over-reaction can result in damage to the tissues that the neutrophil should be programmed to protect.
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Introduction 1 2 References
Their Physiological and Pathobgical Boles
9 other sections not shown
activation adhesion molecules amino acids antibodies antigen arachidonic binding Biochem Biol Biophys blood bone marrow Ca2+ calpain CatG cathepsin cDNA characterization Chem chemotactic chronic granulomatous disease Clin cloning Cockcroft collagenase colony-stimulating factor components cytochrome cytokines cytosol domain elastase endothelial cells endothelium enzyme etal expression FMLP function G proteins gene GM-CSF granules granulocyte HL60 cells human neutrophils Immunol induced inflammation inflammatory inhibited inhibitors integrins interactions interleukin intracellular Invest involved kinase L-selectin leukocytes ligand lipid LTB4 lung lymphocytes macrophages mechanism mediated molecular monocytes mRNA NADPH oxidase Natl Acad neutro nucleotide patients peptide phospholipase phosphorylation PLA2 plasma membrane platelet platelet-activating factor polymorphonuclear prime neutrophils Proc production proteases proteinase Purification rabbit receptor regulation release reperfusion respiratory burst response role Segal selectins sequence serine serum signal transduction specific stimulated studies substrate subunit superoxide tissue TNFa tumor necrosis tyrosine vascular vitro vivo
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