Overview

The conceptual basis for molecular mimicry was first defined in the early 1980s when monoclonal antibodies against viruses were also shown to react with non-viral host protein; in this case, measles virus phosphoprotein cross-reacted with host cell cytokeratin, herpes simplex virus type 1 with host-cell vimentin and vaccinia virus with host-cell intermediate filaments. Following this discovery, others emerged, again at the clonal level, that T cell clones against proteins from a variety of infectious agents also reacted with host antigenic determinants. The clonal distinction was imperative for the initial definition of mimicry. At least 30 years prior to our initial description of molecular mimicry involving cross-reactions between numerous microbes, on the polyclonal antibody level, streptococcus was believed to react with renal glomeruli, heart and basal ganglia to account for the glomerulonephritis, heart and valvular disease and chorea, respectively. However, subsequent research showed that the nephritis was caused by immune complex deposits and the tissue damage they produced. Later, in 1990, the cross-reactivity of streptococcal antigen with myocardial antigens on a clonal level was uncovered. Hence, for both historical reasons and mechanistic understanding, it is best to provide evidence for cross-reactivity at the clonal level to prove that molecular mimicry exists.

Full Product Details

Author:   Michael B. A. Oldstone
Publisher:   Springer-Verlag Berlin and Heidelberg GmbH & Co. KG
Imprint:   Springer-Verlag Berlin and Heidelberg GmbH & Co. K
Edition:   2005 ed.
Volume:   296
Dimensions:   Width: 15.50cm , Height: 1.20cm , Length: 23.50cm
Weight:   0.475kg
ISBN:  

9783540255970

ISBN 10:   3540255974
Pages:   168
Publication Date:   03 November 2005
Audience:   Professional and scholarly ,  Professional & Vocational
Format:   Hardback
Publisher's Status:   Active
Availability:   Out of stock  
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Table of Contents

Molecular Mimicry, Microbial Infection, and Autoimmune Disease: Evolution of the Concept.- The Structural Interactions Between T Cell Receptors and MHC-Peptide Complexes Place Physical Limits on Self-Nonself Discrimination.- A Virus-Induced Molecular Mimicry Model of Multiple Sclerosis.- Suppression of Autoimmunity via Microbial Mimics of Altered Peptide Ligands.- Molecular and Cellular Mechanisms, Pathogenesis, and Treatment of Insulin-Dependent Diabetes Obtained Through Study of a Transgenic Model of Molecular Mimicry.- Trypanosoma cruzi-Induced Molecular Mimicry and Chagas’ Disease.- HTLV-1 Induced Molecular Mimicry in Neurological Disease.- Molecular Mimicry: Anti-DNA Antibodies Bind Microbial and Nonnucleic Acid Self-Antigens.- Chlamydia and Antigenic Mimicry.

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