Molecular Mimicry, Microbial Infection, and Autoimmune Disease: Evolution of the Concept
Open accessAbstract
Molecular mimicry is defined as similar structures shared by molecules from dissimilar genes or by their protein products. Either several linear amino acids or their conformational fit may be shared, even though their origins are separate. Hence, during a viral or microbe infection, if that organism shares cross-reactive epitopes for B or T cells with the host, then the response to the infecting agent will also attack the host, causing autoimmune disease. A variation on this theme is when a second, third, or repeated infection(s) shares cross-reactive B or T cell epitopes with the first (initiating) virus but not necessarily the host. In this instance, the secondary infectious agents increase the number of antiviral/antihost effector antibodies or T cells that potentiate or precipitate the autoimmune assault. The formation of this concept initially via study of monoclonal antibody or clone T cell cross-recognition in vitro through its evolution to in vivo animal models and to selected human diseases is explored in this mini-review.
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Evolution of molecular mimicry between gut bacteria and the host can affect host eating behavior.
“These ground-breaking findings posit that evolution of molecular mimicry between gut bacteria and the host (Oldstone, 2005) can affect host eating behavior.”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Oldstone, 2005
The paper’s introductory passage describes molecular mimicry between microbes and hosts, and its References list examples involving bacteria. It does not say that mimicry evolved between gut bacteria and hosts or that it affects eating behavior; the title’s “evolution” refers to the development of the concept. (LLM, conf=0.82)
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Pathogenesis of Human Coronaviruses Other than Severe Acute Respiratory Syndrome Coronavirus
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miPepBase: A Database of Experimentally Verified Peptides Involved in Molecular Mimicry
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- Authors
- Oldstone, M. B. A.
- Affiliations
- Scripps Research Institute (US)
- Corresponding author
- Oldstone, M. B. A.
- ORCID
- Oldstone, M. B. A.
- Venue
- Current Topics in Microbiology and Immunology
- Publisher
- Springer Berlin Heidelberg
- Published
- 2005
- Volume
- 296
- Pages
- 1-17
- ISSN
- 0070-217X (ISSN-L)
- PMC
- PMC7120699
- OpenAlex
- W96814828
- Cited by
- 146
- References
- 53
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 4 · 2022: 7 · 2021: 9 · 2020: 5 · 2019: 7 · 2018: 5 · 2017: 6 · 2016: 5 · 2015: 5 · 2014: 13 · 2013: 17 · 2012: 6
- FWCI
- 8.50
- Type
- book chapter
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Current topics in microbiology and immunology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (AI045927, R01AI045927, AI036222, R01AI036222, AI-009484)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK058541, DK-058541)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Rheumatology › Systemic Lupus Erythematosus Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › vaccines and immunoinformatics approaches
- Keywords
- molecular mimicry, autoimmune disease, microbial infection, cross-reactive epitopes, B-cell epitopes, T cell epitopes, viral infection, secondary infection, autoimmunity, monoclonal antibodies, animal models of autoimmunity
- MeSH terms
- Amino Acid Sequence, Animals, Epitopes, Autoantibodies, Autoantigens, Autoimmune Diseases, Disease Models, Animal, Humans, Infections, Molecular Sequence Data, T-Lymphocytes, Models, Immunological, Molecular Mimicry
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