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Our main research goal is to understand the molecular mechanisms causing inflammation, particularly in Ankylosing Spondylitis and other forms of inflammatory arthritis, and to translate this understanding into new patient therapy.

Ankylosing spondylitis (AS) is a chronic condition which affects primarily the joints of the lower back. 'Ankylosing' means stiffening and 'spondylitis' means inflammation of the spine; people with this condition suffer from back pain and stiffness, fatigue, and pain and swelling in other parts of the body. Currently, there is no cure for AS, but some treatments relieve symptoms of the condition and may possibly prevent its progression.

Development of a number of common forms of inflammatory arthritis (the spondyloarthritides), which include Ankylosing Spondylitis is strongly associated with possession of the Human Leukocyte Antigen (HLA) class I allele HLA-B27.

Despite extensive studies, the pathogenic role of HLA-B27 in the spondyloarthritides remains unknown.

We hypothesize that the role of HLA-B27 in spondyloarthropathy stems from its function in antigen presentation, either in peptide selection and binding or in other aspects of its cell biology.

We first described the ability of HLA-B27 to form homodimers and have shown that these homodimers are present on the surface of spondyloarthritis patients' cells as well as in B27 transgenic models of disease.

We have defined a number of cellular receptors for B27 homodimers including KIR3DL2. Notably greatly increased numbers of T and NK cells from patients with spondyloarthritides express KIR3DL2.

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