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SUMMARY:Why does HLA-B27 predispose to autoimmune Spondyloarthritis? - Dr 
 Paul Bowness\, MRC Human Immunology Unit\, Institute of Molecular Medicine
 \, University of Oxford
DTSTART:20090520T113000Z
DTEND:20090520T123000Z
UID:TALK17897@talks.cam.ac.uk
CONTACT:Prof. Jim Kaufman
DESCRIPTION:Paul Bowness studies the role of the Human Leukocyte Antigen (
 HLA) class I allele HLA B27 in the pathogenesis of spondyloarthritis.\n\nH
 LA B27 forms a complex with beta 2 microglobulin (ß2m) and binds antigeni
 c peptides within cells. These complexes then travel to the cell surface w
 here 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 fr
 om its function in antigen presentation\, either in peptide selection or o
 ther aspects of its cell biology\, for example its propensity to form homo
 dimers.\n\nHLA B27 heavy chains can also form stable homodimers lacking ß
 2m\, both in vitro and in vivo. These homodimers are expressed at the cell
  surface\, and for this disulphide bonding is critical. We are currently i
 nvestigating possible mechanisms by which HLA B27 homodimers could be dire
 ctly involved in disease pathogenesis. We have recently shown that tetrame
 ric complexes of HLA B27 homodimers bind to Natural Killer and related imm
 unoreceptors on populations of lymphocytes\, monoocytes and natural killer
  cells from patients with spondyloarthritis.\n\n
LOCATION:Lecture Theatre\, Department of Pathology\, Tennis Court Road
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