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Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
Published on: February 22, 2019
HLA-B27 and host-pathogen interaction.
Anna S Sahlberg1, Kaisa Granfors, Markus A Penttinen
1Department of Bacterial and Inflammatory Diseases, National Public Health Institute, Turku, Finland.
Advances in Experimental Medicine and Biology
|September 8, 2009
Summary
Human Leukocyte Antigen B27 (HLA-B27) may influence reactive arthritis development by altering host-bacterial interactions. Its unique properties, like misfolding, could trigger cellular stress favoring infection.
Area of Science:
- Immunogenetics
- Rheumatology
- Microbiology
Background:
- Human Leukocyte Antigen B27 (HLA-B27) is a significant risk factor for spondyloarthropathies (SpA), including reactive arthritis (ReA).
- Reactive arthritis develops following specific bacterial infections, affecting primarily HLA-B27 positive individuals.
- The precise mechanisms linking HLA-B27 to infection-triggered ReA remain incompletely understood.
Purpose of the Study:
- To explore the role of HLA-B27 in modulating host-bacterial interactions during reactive arthritis pathogenesis.
- To discuss potential mechanisms by which HLA-B27 influences the development of infection-triggered SpA.
Main Methods:
- Review and synthesis of existing observational data on HLA-B27 and reactive arthritis.
- Analysis of proposed molecular mechanisms involving HLA-B27's unique properties.
Main Results:
- HLA-B27's antigen-presenting function is considered alongside its unusual properties, such as heavy chain misfolding and homodimer formation in the endoplasmic reticulum (ER).
- These properties may induce ER stress signaling pathways within host cells.
- Such cellular stress responses could potentially create an environment conducive to ReA-triggering bacteria.
Conclusions:
- HLA-B27 likely plays a critical role beyond antigen presentation in the pathogenesis of reactive arthritis.
- Misfolding and ER stress induced by HLA-B27 may represent key mechanisms modulating host-bacterial interactions in ReA.
- Further research into these mechanisms could reveal novel therapeutic targets for SpA.
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