Christopher Buckley

Senior Clinical Research Fellow, Director of Clinical Research

Chris Buckley obtained his first degree in Biochemistry from the University of Oxford (1985) with subsequent undergraduate training in Medicine at the Royal Free Hospital, London (1990).

His postgraduate medical training was in General Medicine and Rheumatology at the Hammersmith Hospital, London (Professors Mark Walport and Dorian Haskard), and John Radcliffe Hospital, Oxford. He obtained a DPhil (arising from a Wellcome Trust Clinical Training Fellowship) with Professor John Bell and Dr David Simmons at the Institute Molecular Medicine, Oxford.

In 1996, funded by a Wellcome Trust Clinician Scientist Fellowship, he joined the Department of Rheumatology in Birmingham. In 2001, he was awarded an MRC Senior Clinical Fellowship and in 2002 became Arthritis Research UK Professor of Rheumatology. In 2012, he was appointed Director of the Birmingham NIHR Clinical Research Facility. And in May 2017, he was appointed as Kennedy Professor of Translational Rheumatology.

In this joint academic post as Director of Clinical Research at the Kennedy Institute in Oxford and Director of NIHR Infrastructure for Birmingham Heath Partners he will lead the Arthritis Therapy Acceleration Programme (A-TAP) which aims to deliver “stratified pathology” in a range of immune mediated inflammatory diseases in order to choose the right disease indication for the right drug.

This approach complements stratified medicine where the aim is to choose the right drug for the right patient. As part of the Stromal Cell group at the Kennedy, his laboratory explores the role of fibroblasts in driving disease progression and tissue tropism in Rheumatoid Arthritis.

Recent Publications

Gain-of-Function Mutation of Tristetraprolin Impairs Negative Feedback Control of Macrophages In Vitro yet Has Overwhelmingly Anti-Inflammatory Consequences In Vivo.
O'Neil JD. et al, (2017), Mol Cell Biol, 37
Treatment of inflammatory arthritis via targeting of tristetraprolin, a master regulator of pro-inflammatory gene expression.
Ross EA. et al, (2017), Ann Rheum Dis, 76, 612 - 619
Decrease in articular hypoxia and synovial blood flow at early time points following infliximab and etanercept treatment in rheumatoid arthritis.
Fisher BA. et al, (2016), Clin Exp Rheumatol, 34, 1072 - 1076
Detection of antibodies to citrullinated tenascin-C in patients with early synovitis is associated with the development of rheumatoid arthritis.
Raza K. et al, (2016), RMD Open, 2
Dual-Specificity Phosphatase 1 and Tristetraprolin Cooperate To Regulate Macrophage Responses to Lipopolysaccharide.
Smallie T. et al, (2015), J Immunol, 195, 277 - 288