PhD, BSc (Hons)
Professor of Gene Medicine
- Head of NDCLS
Gene Therapy for Lung diseases
Deborah Gill is based in the John Radcliffe Hospital in Oxford where she is Professor of Gene Medicine, Co-Director of the Gene Medicine Research Group and Head of the Nuffield Division of Clinical Laboratory Sciences within the Radcliffe Department of Medicine at the University of Oxford.
Deborah completed her PhD in molecular microbiology at the University of Warwick, studying cell division proteins in E.coli, during which she discovered the defining bacterial member of the ABC (ATP-Binding Cassette) superfamily of proteins. Deborah then moved to the University of Oxford, to undertake post-doctoral research at the Weatherall Institute for Molecular Medicine, investigating human ABC proteins including the Multi-Drug Resistance p-glycoprotein and CFTR, the protein responsible for Cystic Fibrosis (CF). Deborah's research then began to focus on the potential of gene therapy for genetic diseases, developing a potential treatment for Cystic Fibrosis lung disease, and resulting in multiple clinical trials demonstrating proof of principle for CF gene therapy.
Deborah was a founding member of the UK CF Gene Therapy Consortium in 2001, a consortium of scientists and clinicians that continues to work toward making gene therapy a reality for patients with CF. Since the success of gene therapy ultimately depends on efficient delivery of genetic material to human cells, Deborah's research team has focused on the development of new viral and non-viral gene transfer vectors for translation of gene therapies to the clinic. In addition to targeting genetic diseases in the lung (such as Surfactant-Deficiencies) Deborah's research team is evaluating whether the airways can be used as a "protein factory" to make therapeutic proteins and antibodies.
Repeated nebulisation of non-viral CFTR gene therapy in patients with cystic fibrosis: a randomised, double-blind, placebo-controlled, phase 2b trial.
Alton EWFW. et al, (2015), Lancet Respir Med, 3, 684 - 691
CpG-free plasmids confer reduced inflammation and sustained pulmonary gene expression.
Hyde SC. et al, (2008), Nat Biotechnol, 26, 549 - 551
Type I interferon signaling deficiency results in dysregulated innate immune responses to SARS-CoV-2 in mice.
Ogger PP. et al, (2022), Eur J Immunol
Sendai F/HN pseudotyped lentiviral vector transduces human ciliated and non-ciliated airway cells using α 2,3 sialylated receptors
Munday RJ. et al, (2022), Molecular Therapy - Methods and Clinical Development, 26, 239 - 252
Progress in Respiratory Gene Therapy.
McLachlan G. et al, (2022), Hum Gene Ther, 33, 893 - 912
Correction of a chronic pulmonary disease through lentiviral vector-mediated protein expression
Lund-Palau H. et al, (2022), Molecular Therapy - Methods and Clinical Development, 25, 382 - 391
A High-Throughput Cell Culture Model of Idiopathic Pulmonary Fibrosis (IPF) for Gene Therapy Applications
Cerezuela MP. et al, (2022), MOLECULAR THERAPY, 30, 292 - 292