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HLA-B27 and Host-Pathogen Interaction

  • Chapter
Molecular Mechanisms of Spondyloarthropathies

Part of the book series: Advances in Experimental Medicine and Biology ((volume 649))

Abstract

HLA-B27 is a risk factor closely associated to spondyloarthropathies (SpA). One form of SpA is reactive arthritis (ReA), which develops as a complication after certain bacterial infections (e.g., Salmonellae, Yersiniae, Shigellae, Campylobacteriae. and Chlamydiae). The development of infection-triggered complication is a complex train of events between the triggering bacteria and the host. Since most of the patients suffering from ReA are HLA-B27 positive, it has been proposed that HLA-B27 may modulate the interaction between ReA-triggering bacteria and host cell. Besides antigen presenting function, HLA-B27 displays other unusual properties that might be of importance in the development of ReA. These properties (homodimer formation and misfolding of HLA-B27 heavy chain in the endoplasmic reticulum (ER) may trigger ER-strees signaling pathways in host cell, which in turn may modulate cell signaling in favor of ReA-triggering bacteria. Here we summarize the observations of HLA-B27 modulating the interaction between ReA-triggering bacteria and host cell and discuss potential mechanisms behind the interaction.

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Authors and Affiliations

  1. Department of Bacterial and Inflammatory Diseases, National Public Health Institute, Turku, Finland

    Anna S. Sahlberg & Kaisa Granfors

  2. Department of Medical Microbiology and Immunology, University of Turku, Kiinamyllynkatu 13, FIN-20520, Turku, Finland

    Markus A. Penttinen

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  1. Anna S. Sahlberg
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  2. Kaisa Granfors
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  3. Markus A. Penttinen
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Editors and Affiliations

  1. Hospital Universitario Central de Asturias, Oviedo, Spain

    Carlos López-Larrea PhD  & Roberto Díaz-Peña BSc  & 

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Sahlberg, A.S., Granfors, K., Penttinen, M.A. (2009). HLA-B27 and Host-Pathogen Interaction. In: López-Larrea, C., Díaz-Peña, R. (eds) Molecular Mechanisms of Spondyloarthropathies. Advances in Experimental Medicine and Biology, vol 649. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-0298-6_17

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