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Published on: September 26, 2012
Molecular mimicry--hypothesis or reality?
1Department of Medicine and Physical Therapy, University of Tokyo School of Medicine, Japan.
Abstract:
A number of observations support molecular mimicry as a possible pathogenetic mechanism in diseases such as acute rheumatic fever, reactive arthritis after enteric infection or associated with Reiter's syndrome, myasthenia gravis, or even in rheumatoid arthritis. Molecular mimicry can be defined as a sharing of epitopes in linear or 3-dimensional presentation on disparate proteins from entirely different sources--for instance, group A streptococcal membranes and human cardiac myosin. How exposure to or infection with organisms sharing molecular similarity with antigens of the human host can evade tolerance and actually induce a self-reacting humoral or cellular immune response is still not clear; however, a large body of evidence has now been accumulated that documents apparent molecular mimicry mechanisms in these disorders. In some diseases, the molecular mimicry appears to involve human target organs and specific components of the infectious organism, whereas in others the host HLA cell surface molecules appear to share antigens with presumed bacterial or viral initiators of disease.
Insights
Molecular mimicry, where microbes resemble human proteins, may trigger autoimmune diseases like rheumatic fever and rheumatoid arthritis. This mechanism explains how infections can lead to self-attacking immune responses.
Area of Science:
- Immunology
- Pathogenesis
- Autoimmune Diseases
Background:
- Molecular mimicry is a proposed mechanism in various autoimmune disorders.
- It involves the sharing of similar epitopes between microbial and host antigens.
- Examples include acute rheumatic fever, reactive arthritis, myasthenia gravis, and rheumatoid arthritis.
Purpose of the Study:
- To explore the role of molecular mimicry in autoimmune disease pathogenesis.
- To define the concept and mechanisms of molecular mimicry.
- To review evidence supporting molecular mimicry in specific diseases.
Main Methods:
- Review of existing scientific literature and observations.
- Analysis of epitope sharing between microbial and human proteins.
- Examination of host immune responses in the context of infection.
Main Results:
- Evidence supports molecular mimicry as a pathogenic mechanism in several autoimmune diseases.
- Molecular mimicry involves shared epitopes on microbial and human proteins.
- Mechanisms include mimicry of target organs or host HLA molecules.
Conclusions:
- Molecular mimicry is a significant factor in the development of certain autoimmune diseases.
- Further research is needed to fully elucidate the mechanisms of immune evasion and self-reactivity.
- Understanding molecular mimicry offers potential therapeutic targets for autoimmune conditions.
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