By Michael B.A. Oldstone (Editor)
The conceptual foundation for molecular mimicry used to be first outlined within the early Nineteen Eighties while monoclonal antibodies opposed to viruses have been additionally proven to react with non-viral host protein; consequently, measles virus phosphoprotein cross-reacted with host telephone cytokeratin, herpes simplex virus variety 1 with host-cell vimentin and vaccinia virus with host-cell intermediate filaments. Following this discovery, others emerged, back on the clonal point, that T cellphone clones opposed to proteins from quite a few infectious brokers additionally reacted with host antigenic determinants. The clonal contrast used to be principal for the preliminary definition of mimicry. no less than 30 years ahead of our preliminary description of molecular mimicry regarding cross-reactions among a variety of microbes, at the polyclonal antibody point, streptococcus was once believed to react with renal glomeruli, middle and basal ganglia to account for the glomerulonephritis, center and valvular affliction and chorea, respectively. besides the fact that, next examine confirmed that the nephritis was once as a result of immune advanced deposits and the tissue harm they produced. Later, in 1990, the cross-reactivity of streptococcal antigen with myocardial antigens on a clonal point used to be exposed. for this reason, for either historic purposes and mechanistic realizing, you should supply facts for cross-reactivity on the clonal point to turn out that molecular mimicry exists.
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Additional resources for Current Topics in Microbiology and Immunology, Volume 296, Molecular Mimicry: Infection Inducing Autoimmune Disease, 1st Edition
47 5 Infection of the Target Organ Is Not Required for Autoimmune Disease Induced by Molecular Mimicry . . . . . . . . . . . . . . . 47 6 Model for Molecular Mimicry Induced Autoimmune Demyelinating Disease . . . . . . . . . . 48 7 Conclusions and Perspectives . . . . . . . . . . . . . . . . 50 References . . . . . . . . . . . . . . . . . . . . . . . . . 51 Abstract Multiple sclerosis1 (MS) is an immune-mediated autoimmune demyelinating disease in humans.
Proc. Natl. Acad. Sci. E. 1993. Degenerate recognition of a dissimilar antigenic peptide by myelin basic protein-reactive T cells. Implications for thymic education and autoimmunity. J. Immunol. K. 2002. T cell immunodominance and maintenance of memory regulated by unexpectedly cross-reactive pathogens. Nat. Immunol. C. 1993. Three-dimensional structure of the human class II histocompatibility antigen HLA-DR1. J. 1994. An alloresponse in humans is dominated by cytotoxic T lymphocytes (CTL) cross-reactive with a single EpsteinBarr virus CTL epitope: implications for graft-versus-host disease.
To determine whether the nonpathogenic ∆Cla-TMEV could serve as a vector to test the potential of infection-induced molecular mimicry to initiate CNS autoimmunity, we inserted the coding region for immunodominant encephalitogenic myelin antigen, PLP139–151 , as a 30-amino acid insertion, PLP130–159 (Fig. 1) using the ClaI restriction site. The the 30-mer rather than the minimal encephalitogenic epitope was used to ensure that disease could only be induced if the T cell determinant was correctly processed from its ﬂanking residues in the context of the virus infection.