By Kenneth Michael Pollard
This is often the 1st e-book to handle all elements of the biology of autoantibodies in one quantity, together with a dialogue of immunology, experimental types, medical points, and using autoantibodies as probes in molecular and mobile biology. The editor, at the moment professor on the W.M. Keck Autoimmune sickness middle of The Scripps learn Institute, has assembled an all-star crew of authors to record at the most modern learn, applied sciences, and purposes. Following an introductory bankruptcy, the booklet is going directly to conceal such issues as mobile mechanisms of autoantibody creation, medical and diagnostic usefulness in human affliction, and animal types used to check the elicitation of autoantibodies. the total is rounded off with a glance at destiny views. With its finished insurance, this quantity will charm not just to immunologists and clinicians but additionally to mobile and molecular biologists.
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Extra resources for Autoantibodies and Autoimmunity: Molecular Mechanisms in Health and Disease
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2002. Phosphatidylserine-dependent ingestion of apoptotic cells promotes TGF-beta1 secretion and the resolution of inflammation. J Clin Invest 109:41–50. , B. Krammer, and G. Schwamberger. 1999. Cutting edge: differential effect of apoptotic versus necrotic tumor cells on macrophage antitumor activities. J Immunol 163:1730–1732. Pollard, K. , D. L. Pearson, M. Bluthner, and E. M. Tan. 2000. Proteolytic cleavage of a self-antigen following xenobiotic-induced cell death produces a fragment with novel immunogenic properties.
The significance of IFN-c in systemic autoimmunity has been demonstrated in non-autoimmune-prone mice made transgenic for IFN-c expression in the epidermis . The increased expression of IFN-c leads to a lupus-like disease characterized by production of autoantibodies and immune complex– mediated tissue damage . Further evidence for the importance of IFN-c has come from an examination of gene expression in the Nba2 locus of chromosome 1 of the mouse. Nba2 is a genetic interval identified as a locus of genetic susceptibility for lupus in the NZB strain.