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Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
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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
PubMed

Insights

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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