Related Experiment Videos
Molecular mimicry in the pathogenesis of rheumatic diseases
1Arthritis Research Center, University of Texas Health Sciences Center at Dallas, Southwestern Medical School.
Abstract:
Evidence has been presented to support the conclusion that epitope-specific cross-reactive autoimmunity generated in response to a microorganism can result in an inflammatory sequela. The role of this mechanism in the pathogenesis of the experimental disease, adjuvant arthritis, appears clear. In the case of human rheumatic conditions, such as rheumatic fever and the HLA-B27-associated reactive arthritides, the role is not yet established, but clinical evidence suggests that the hypothesis is an attractive one.
Insights
Microorganism-induced autoimmunity may cause inflammation. This mechanism is clear in experimental arthritis and suggested by clinical evidence in human rheumatic diseases like reactive arthritis.
Area of Science:
- Immunology
- Rheumatology
- Pathogenesis
Background:
- Epitope-specific cross-reactive autoimmunity can arise from microbial infections.
- This immune response is a potential cause of inflammatory conditions.
Purpose of the Study:
- To explore the role of cross-reactive autoimmunity in inflammatory sequelae.
- To investigate this mechanism in adjuvant arthritis and human rheumatic diseases.
Main Methods:
- Review of existing evidence on autoimmunity and inflammation.
- Analysis of experimental models (adjuvant arthritis).
- Clinical observation in human rheumatic conditions (rheumatic fever, reactive arthritides).
Main Results:
- The mechanism is clearly implicated in the pathogenesis of adjuvant arthritis.
- Clinical data suggests the hypothesis is plausible for human rheumatic conditions.
Conclusions:
- Cross-reactive autoimmunity is a significant factor in experimental inflammatory diseases.
- Further research is warranted to confirm its role in human rheumatic diseases such as reactive arthritis.