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

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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.

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