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SUMMARY:The role of KIR3DL2 HLA-B27 interactions in inflammatory arthritis
  - symptom or cause? - Dr Simon Kollnberger\, University of Oxford
DTSTART:20130313T123000Z
DTEND:20130313T133000Z
UID:TALK41803@talks.cam.ac.uk
CONTACT:Sue Griffin
DESCRIPTION:The role of KIR3DL2 HLA-B27 interactions in inflammatory arthr
 itis - symptom or cause?\n\nWe have shown that KIR3DL2 expressing CD4 T ce
 lls\, highly enriched for IL-23 receptor and producing IL-17 are expanded 
 in spondyloarthritis.  We have also observed expansions of KIR3DL2-express
 ing NK cells in spondyloarthritis patients. The unfolded protein response 
 hypothesis proposes that arthritis is promoted by HLA-B27 misfolding in th
 e ER stimulating production of inflammatory cytokines including IL-23. \n\
 nThe question we are currently addressing is whether IL23 or HLA-B27-KIR3D
 L2 interactions drive the differentiation of KIR3DL2-expressing leukocytes
  in arthritis. \n
LOCATION:Lecture Theatre\, Department of Pathology\, Tennis Court Road
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