The Epigenetics of Autoimmune Diseases (Hardcover, New)

The role of epigenetic mechanisms in autoimmune disease is only now starting to become clear. Understanding these mechanisms, their effect on cellular function and the role of environmental factors is vital to determining how to manage these often debilitating and fatal diseases. Drawing on the research of leading experts, this book provides a valuable insight into this important new area of autoimmunity research and a clear, up-to-date view on the major advances in the field. Specific coverage includes: How highly developed epigenetic mechanisms are involved in several aspects of normal immune regulation, in addition to maintaining immune tolerance to self-determinants. Specific epigenetic aspects of human autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, autoimmune diabetes, thyroid autoimmunity, inflammatory bowel disease and autoimmune hepatitis. How understanding epigenetic mechanisms can lead to therapeutic strategies based on manipulation of this previously unexploited facet of immune regulation. Discussion of the novel approaches that are being investigated to prevent or treat autoimmune diseases. This book is an essential resource for those actively involved in the field. It is also of interest to basic researchers interested in understanding the origin of autoimmunity and clinical specialists interested in gaining in-depth understanding of the pathogenesis of autoimmune diseases and their treatment.

General

Imprint:	John Wiley & Sons
Country of origin:	United States
Release date:	April 2009
First published:	October 2009
Authors:	M. Zouali
Dimensions:	252 x 174 x 30mm (L x W x T)
Format:	Hardcover
Pages:	472
Edition:	New
ISBN-13:	978-0-470-75861-8
Categories:	Books > Medicine > Pre-clinical medicine: basic sciences > Medical genetics Books > Medicine > Clinical & internal medicine > Diseases & disorders > Immunology > General Promotions
LSN:	0-470-75861-9
Barcode:	9780470758618

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