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Apoptosis and inflammation. Ed James D Winkler. (Pp 256; DM228.) Basel: Birkhäuser Verlag, 1999. ISBN 3-7643-5795-9.
Apoptosis is one of the hottest topics in present day research, offering an umbrella for studies in the fields of general biochemistry, cell biology, cellular differentiation, molecular biology, and immunology. A few years ago it became clear that there is also a strong link between apoptosis and autoimmunity. In some autoimmune diseases it has been shown that there is a defect at some step in the apoptotic cascade of events which, in genetically susceptible people, may lead to a change in the delicate equilibrium between life and death of certain cells. Such a lack of balance may ultimately be the cause of either too much cell death or too little. Similarly, many studies have shown that autoantigens become modified during apoptosis, and that these modified antigens are translocated to the blebs at the periphery of the cell. It is likely, although not proved, that exposure of such modifications may ultimately lead to the generation of autoantibodies. One of the intrinsic possibilities of such a mechanism could be that the (disturbed) apoptosis of a specific cell type might lead to a localised inflammation and a local production of a certain autoantibody. Such a mechanism could provide an explanation for the often observed specificity of autoantibody production in a specific disease.
Apoptosis and Inflammation offers an excellent overview of apoptosis in different cells important for the process of inflammation, and its possible role in certain inflammatory diseases. There are two chapters on signals for apoptosis important to inflammatory cells—namely, growth factors and arachidonic acid metabolism. Next, the book focuses on effects at the cellular level, on cell survival versus death and signals critical for cell function in both normal and disease states. This part contains very informative reviews on apoptosis of lymphocytes, chondrocytes, and keratinocytes. Finally, it focuses on events at the level of tissue and disease, looking at the evidence for altered apoptosis in inflammatory diseases such as rheumatoid arthritis, osteoarthritis, lupus, and renal disease.Together these chapters provide a timely and extensive overview of the state of the art, not only for the scientist working in the field of apoptosis but also for the clinician who wants a better insight into disease.
From an educational viewpoint it is a pity that only a few schematic figures have been included. Most of the chapters are primarily text containing many references and thus require a deal of endurance from the reader. For example, there is only one figure, in the middle of the book, which gives a schematic overview of the most common pathways leading to activation of caspases and apoptosis. Since these pathways have a decisive role in the understanding of most chapters it would have been appropriate to have included an introductory chapter discussing the details of the various mechanisms of apoptosis.
However, for those who are familiar with these mechanisms, this is a fine book that has much to offer.
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