A lecture taking place at the Crick.

: Targeting fibroblast subsets in inflammation and tissue damage


Christopher Buckley

Kennedy Professor of Rheumatology, Kennedy Institute, Oxford and Institute of Inflammation and Ageing, Birmingham

Career summary

I obtained a degree in Biochemistry from the University of Oxford (1985) with subsequent undergraduate training in Medicine (MBBS) at the Royal Free Hospital, London (1990). My postgraduate medical training was in General Medicine and Rheumatology at the Hammersmith Hospital, London (Mark Walport, Dorian Haskard), and John Radcliffe Hospital, Oxford. I obtained a DPhil arising from a Wellcome Trust Clinical Training Fellowship with John Bell and David Simmons at the Institute Molecular Medicine, Oxford in 1996. Funded by a Wellcome Trust Clinician Scientist Fellowship, I joined the Department of Rheumatology in Birmingham later that year. In 2001 I was awarded an MRC Senior Clinical Fellowship and in 2002 became Arthritis Research UK Professor of Rheumatology. In 2012 I was appointed Director of the Birmingham NIHR Clinical Research Facility. In May 2017 I took up a new joint academic post between the Universities of Birmingham and Oxford as Director of Clinical Research at the Kennedy Institute of Rheumatology Oxford and Director of NIHR Infrastructure in Birmingham for Birmingham Health Partners to Direct the Arthritis Therapy Acceleration Programme  (A-TAP)

Targeting fibroblast subsets in inflammation and tissue damage

A characteristic feature of chronic inflammatory reactions is their persistence and predilection for certain anatomical sites. Over the last ten years my group has demonstrated that tissue resident stromal cells (fibroblasts) are important in determining both the switch to persistence as well as the site at which inflammation occurs. In chronic inflammation the resolution phase is delayed and disordered leading to the persistent accumulation of an inflammatory infiltrate. Our work has allowed us to propose that different subsets of fibroblasts exist within tissues; each with non-overlapping functions and which are responsible for the wide variety of tissue driven processes such as immune cell modulation and damage. Our hypothesis predicts that these subsets become disordered during inflammation, leading either to the accumulation of lymphocytes in structures that resemble lymphoid tissues or tissue fibrosis and damage.  We have proposed that inflammation is not generic but contextual and therefore differences in the response of different inflammatory diseases to therapy are likely to be due to intrinsic differences in the behavior of fibroblast subsets within different microenvironments. We suggest that stromal cells in general and fibroblasts in particular offer a new family of organ specific targets to treat chronic immune mediated inflammatory diseases.

Hosted by Brigitta Stockinger

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