Why does HLA-B27 predispose to autoimmune Spondyloarthritis?

Add to your list(s) Download to your calendar using vCal

• Dr Paul Bowness, MRC Human Immunology Unit, Institute of Molecular Medicine, University of Oxford
• Wednesday 20 May 2009, 12:30-13:30
• Lecture Theatre, Department of Pathology, Tennis Court Road.

If you have a question about this talk, please contact Prof. Jim Kaufman.

Host: John Trowsdale (jt233@cam.ac.uk)

Paul Bowness studies the role of the Human Leukocyte Antigen (HLA) class I allele HLA B27 in the pathogenesis of spondyloarthritis.

HLA B27 forms a complex with beta 2 microglobulin (ß2m) and binds antigenic peptides within cells. These complexes then travel to the cell surface where they can be recognised by cytotoxic T lymphocytes which then kill the infected cell. Despite extensive studies, the pathogenic role of HLA B27 remains unknown. The role of HLA B27 in spondyloarthropathy might stem from its function in antigen presentation, either in peptide selection or other aspects of its cell biology, for example its propensity to form homodimers.

HLA B27 heavy chains can also form stable homodimers lacking ß2m, both in vitro and in vivo. These homodimers are expressed at the cell surface, and for this disulphide bonding is critical. We are currently investigating possible mechanisms by which HLA B27 homodimers could be directly involved in disease pathogenesis. We have recently shown that tetrameric complexes of HLA B27 homodimers bind to Natural Killer and related immunoreceptors on populations of lymphocytes, monoocytes and natural killer cells from patients with spondyloarthritis.

This talk is part of the Immunology in Pathology series.

This talk is included in these lists:

• Biology
• Cambridge Immunology
• Cambridge Infectious Disease
• Cambridge Infectious Diseases
• Lecture Theatre, Department of Pathology, Tennis Court Road
• Life Sciences
• Life Sciences
• ME Seminar
• Pathology Seminars
• my_list
• other talks

Note that ex-directory lists are not shown.