The role of KIR3DL2 HLA-B27 interactions in inflammatory arthritis - symptom or cause?

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

• Dr Simon Kollnberger, University of Oxford
• Wednesday 13 March 2013, 12:30-13:30
• Lecture Theatre, Department of Pathology, Tennis Court Road.

If you have a question about this talk, please contact Sue Griffin.

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

The role of KIR3DL2 HLA -B27 interactions in inflammatory arthritis – symptom or cause?

We have shown that KIR3DL2 expressing CD4 T cells, highly enriched for IL-23 receptor and producing IL-17 are expanded in spondyloarthritis. We have also observed expansions of KIR3DL2 -expressing NK cells in spondyloarthritis patients. The unfolded protein response hypothesis proposes that arthritis is promoted by HLA -B27 misfolding in the ER stimulating production of inflammatory cytokines including IL-23.

The question we are currently addressing is whether IL23 or HLA -B27-KIR3DL2 interactions drive the differentiation of KIR3DL2 -expressing leukocytes in arthritis.

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.