Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Dr Sherlock joins the Kennedy Institute to lead a new research group examining the immunobiology of spondyloarthropathy

The Kennedy Institute would like to welcome Dr Jonathan Sherlock, who joins the Institute as a Senior Clinical Research Fellow funded by the Kennedy Trust for Rheumatology Research. Jonathan leads a new research group that will investigate the immunobiology of human spondyloarthropathy. 

Patients with ankylosing spondylitis or other spondyloarthropathies experience joint pain and stiffness. These symptoms are caused by inflammation and abnormal bone growth in the junctions where bones meet tendons called entheses.

Jonathan’s research will examine the molecular and cellular biology of spondyloarthropathy, with a focus on the role of inflammatory cytokines in driving disease. Current treatments for spondyloarthropathies target inflammation, but are not particularly effective at preventing abnormal bone growth. Jonathan’s studies will provide insight into disease pathogenesis, hopefully leading to better treatment options.

Jonathan will collaborate closely with Oxford Investigators Prof Paul Bowness, Prof Fiona Powrie and Prof Peter Taylor, as well as Prof Christopher Buckley (University of Birmingham).  Analysis of patient tissue samples will provide key component of these investigations.

Prior to joining the Kennedy Institute, Jonathan trained with Prof Christopher Buckley and Dr Daniel Cua (Merck Research Laboratories). His research identified a population of the immune cells in the enthesis that drive pathology in a disease model of spondyloarthropathy.

We wish Jonathan all the best in his new position.