Related Experiment Videos
Molecular mimicry: a critical look at exemplary instances in human diseases
1Department of Pathology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA. nrrose@jhsph.edu
Abstract:
Molecular mimicry, the concept that antigenic determinants of microorganisms resemble antigenic determinants of the host, is frequently cited as a plausible mechanism to account for the association of infection and autoimmune disease. Based on analogous sequences of amino acids or on cross-reactions of monoclonal antibodies, numerous examples of such mimicry have been reported. There are, however, no clear examples of a human disease caused by molecular mimicry.
Insights
Molecular mimicry, where microbial antigens resemble host antigens, is a proposed cause for autoimmune diseases. Despite numerous reported examples, no definitive human disease has been clearly linked to this phenomenon.
Area of Science:
- Immunology
- Autoimmunity
- Microbiology
Background:
- Molecular mimicry is a proposed mechanism linking infections to autoimmune diseases.
- This concept is based on similarities between microbial and host antigenic determinants.
- Numerous examples of molecular mimicry have been documented through amino acid sequence analysis and antibody cross-reactivity.
Purpose of the Study:
- To critically evaluate the evidence for molecular mimicry as a cause of human autoimmune diseases.
- To determine if reported instances of molecular mimicry translate to clear etiological links in human pathology.
Main Methods:
- Review of existing literature on molecular mimicry and autoimmune diseases.
- Analysis of reported cases of microbial antigen and host determinant similarities.
- Assessment of antibody cross-reactivity data in the context of human disease.
Main Results:
- Numerous examples of molecular mimicry have been identified based on sequence homology and antibody cross-reactivity.
- Despite these findings, a direct causal link to a specific human autoimmune disease remains unproven.
- The transition from observed mimicry to disease pathogenesis is not clearly established.
Conclusions:
- While molecular mimicry is a plausible hypothesis for autoimmunity, concrete evidence in human diseases is lacking.
- Further research is needed to establish a definitive role for molecular mimicry in the etiology of human autoimmune conditions.