Related Experiment Videos
A ribosomal protein of Yersinia pseudotuberculosis having partial epitope identity with HLA-B27
Abstract:
The phenotype HLA-B27 is common in patients who develop reactive arthritis after having an infection. One hypothesis concerning the pathogenesis of reactive arthritis is that molecular mimicry between HLA-B27 and certain bacterial components might be involved. It is known that an infection with Yersinia is commonly associated with reactive arthritis in B27 positive patients. Therefore, we were interested to investigate whether cross-reactivity between Yersinia and HLA-B27 exists. A gene library of Yersinia pseudotuberculosis was created in the plasmid vector pUC13. One of the resulting clones contained a gene encoding an intracytoplasmic protein that seems to have partial epitope identity with HLA-B27. It reacted in western blot. ELISA and immunoprecipitation with three different HLA-B27 specific monoclonal and polyclonal antibodies of the IgG and IgM class. However DNA-sequencing of the cloned Yersinia gene and the predicted amino acid sequence revealed only a very remote similarity with HLA-B27 in the primary structure. Instead, an extremely high degree of similarity with the ribosomal protein L4 of the S10 operon of Escherichia coli was identified indicating that the protein encoded by the cloned Y. pseudotuberculosis gene is a corresponding ribosomal protein.
Insights
Molecular mimicry between HLA-B27 and Yersinia may cause reactive arthritis. Researchers found a Yersinia protein similar to E. coli ribosomal protein L4, not HLA-B27, challenging this hypothesis.
Area of Science:
- Immunology
- Microbiology
- Genetics
Background:
- Reactive arthritis is linked to HLA-B27 phenotype and infections.
- Molecular mimicry between HLA-B27 and bacterial components is a proposed pathogenesis.
- Yersinia infection is commonly associated with reactive arthritis in HLA-B27 positive individuals.
Purpose of the Study:
- To investigate potential cross-reactivity between Yersinia and HLA-B27.
- To explore the molecular basis of reactive arthritis in HLA-B27 positive patients.
Main Methods:
- Created a Yersinia pseudotuberculosis gene library in a pUC13 plasmid vector.
- Screened clones for proteins with potential epitope identity to HLA-B27 using Western blot, ELISA, and immunoprecipitation.
- Performed DNA sequencing of the cloned Yersinia gene and analyzed the predicted amino acid sequence.
Main Results:
- A Yersinia clone reacted with HLA-B27 specific antibodies, suggesting partial epitope identity.
- DNA sequencing revealed high similarity to Escherichia coli ribosomal protein L4, not HLA-B27.
- The identified protein is a ribosomal protein, challenging the direct molecular mimicry hypothesis.
Conclusions:
- The study identified a Yersinia protein highly similar to E. coli ribosomal protein L4.
- This finding suggests that the observed cross-reactivity may not be due to direct molecular mimicry between Yersinia and HLA-B27.
- Further research is needed to elucidate the exact mechanisms of reactive arthritis pathogenesis in HLA-B27 positive individuals.