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Potential clinical implications of molecular mimicry-induced autoimmunity.
- Source :
-
Immunity, Inflammation & Disease . Feb2024, Vol. 12 Issue 2, p1-16. 16p. - Publication Year :
- 2024
-
Abstract
- Background: Molecular mimicry is hypothesized to be a mechanism by which autoimmune diseases are triggered. It refers to sequence or structural homology between foreign antigens and self-antigens, which can activate cross-reactive lymphocytes that attack host tissues. Elucidating the role of molecular mimicry in human autoimmunity could have important clinical implications. Objective: To review evidence for the role of molecular mimicry in major autoimmune diseases and discuss potential clinical implications. Methods: Comprehensive literature review of clinical trials, observational studies, animal models, and immunology studies on molecular mimicry in multiple sclerosis, type 1 diabetes, rheumatoid arthritis, lupus, Guillain-Barre syndrome, autoimmune myocarditis, and primary biliary cirrhosis published from 2000-2023. Results: Substantial indirect evidence supports molecular mimicry as a contributor to loss of self-tolerance in several autoimmune conditions. Proposed microbial triggers include Epstein-Barr virus, coxsackievirus, Campylobacter jejuni, and bacterial commensals. Key mechanisms involve cross-reactive T cells and autoantibodies induced by epitope homology between microbial and self-antigens. Perpetuation of autoimmunity involves epitope spreading, inflammatory mediators, and genetic factors. Conclusions: Molecular mimicry plausibly explains initial stages of autoimmune pathogenesis induced by infection or microbiota disturbances. Understanding mimicry antigens and pathways could enable improved prediction, monitoring, and antigen-specific immunotherapy for autoimmune disorders. However, definitive proof of causation in humans remains limited. Further research should focus on establishing clinical evidence and utility. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 20504527
- Volume :
- 12
- Issue :
- 2
- Database :
- Academic Search Index
- Journal :
- Immunity, Inflammation & Disease
- Publication Type :
- Academic Journal
- Accession number :
- 177054419
- Full Text :
- https://doi.org/10.1002/iid3.1178