Institute of Cellular Medicine

Staff Profile

Dr Arthur Pratt

Intermediate Clinical Fellow, Honorary Consulatant Rheumatologist


Dr. Arthur G Pratt - BSc, MBChB, MRCP, PhD

Arthur completed his medical training at Leeds Medical School in 2001, with an intercalated BSc degree in Molecular Medicine. After admission to the Royal College of Physicians in 2004 he was awarded an Arthritis Research UK Research Training Fellowship in 2007, having moved to the Newcastle to establish the Northeast Early Arthritis Cohort, and he completed his doctoral studies in 2011. Following a spell as NHIR Clinical Lecturer in Rheumatology, he currently works as an Intermediate Clinical Fellow at Newcastle University. His time is divided between NHS work as an Honorary Consultant Rheumatologist (running the early arthritis service at The Freeman Hospital), clinical trial work, and research (including PhD student supervision) within the Institute of Cellular Medicine.


I am interested in how an improved understanding of the aetiopathogenesis of early rheumatoid arthritis (RA) might improve our ability to diagnose and treat patients with the disease. My research seeks to identify molecular biomarkers that begin to stratify this highly heterogeneous condition into subgroups of clinical significance.

Rheumatoid arthritis is a chronic and highly heterogeneous disease of immune dysregulation characterised by painful and destructive inflammation of synovial joints. Despite a wealth of existing and emerging therapies there is no cure for the condition, which remains a cause of disability, reduced quality of life and increased mortality. An overarching aim in our laboratory is to develop biomarkers that stratify patients according to pathobiology during the earliest clinical stage of RA, potentially enabling more rational therapeutic targeting.

We have developed a well characterised early arthritis inception cohort which has provided a rich resource for observational studies. Genetic investigations increasingly emphasise an orchestrating role for CD4 and B lymphocytes in RA pathogenesis, and our work to date has focused on these cell types: for example, our recent expression quantitative trait locus (eQTL) analysis of CD4 lymphocytes in untreated arthritis patients refined the candidate causal gene landscape of RA. The transcriptome of these cells also points to the importance of interleukin-6 mediated STAT3 signalling as an early event in a diagnostically challenging RA sub-group, and we have validated this finding and continue to investigate its potential implications for the clinic.

Finally, we are increasingly interested in delineating mechanisms of immune dysregulation that are shared between diseases beyond RA, and the opportunities they may afford to re-purpose RA drugs in other conditions and vice versa.