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 DiseaseMolecular Mimicry: Anti-DNA Antibodies Bind Microbial and Nonnucleic Acid Self-Antigens; Chlamydia and Antigenic Mimicry.
SUMMARY OR ABSTRACT
Text of Note
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 fo.