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个人简介

I graduated from the University of Salford in 1994 in Biological and Biochemical science. Following a masters in Immunology & Immunogenetics (University of Manchester), I completed my PhD at the University of Sheffield to study the role of mast cells in allergic disease in the absence of IgE. This study was the initiation of my published career in lung immunology. Post doctoral work in Sunderland and Newcastle focused on ‘tissue restricted lymphocyte’ action during lung transplant rejection. Research was directed to identify and blockade adhesion proteins that facilitated recognition and destruction events during rejection. I then spent 2 years at the Paterson Institute for Cancer Research undertaking studies of T cell responses to HPV in cervical cancer patients and identifying the role of the oncofetal antigen 5T4. Returning to lung immunology, I worked in the University Hospital of South Manchester (UHSM) North West Lung Centre (NWLC) Labs and the Medicines Evaluation Unit (MEU) for 7 years undertaking lab management roles, clinical studies, clinical trials, and collaborative work with industry. Work characterized the pathobiology of respiratory diseases; chronic obstructive pulmonary disease (COPD) and asthma, while pharmacological studies characterized the action of novel therapeutic drugs. From 2010, I accepted a lecturing position (Biomedical Science and Human Physiology) at the University of Salford in the School of Environment & Life Sciences (ELS) where I continue to publish on respiratory disease and enjoy bringing clinical aspects to both teaching and research. My aim is to share my passion with students so they too can better understand pathological processes in disease, and become the next generation of scientists developing improved treatments for patients.

研究领域

1. Lung fibrosis and 'cellular remodelling' events 2. Altered adaptive immunity associated with lung inflammation 1. Lung fibrosis is commonly associated with COPD but can also occur without a cause (idiopathic). Lung epithelia cells normally have the potential to regenerate in response to damage and fibroblasts provide an extracellular scaffold for elasticity. In fibrotic disease this regeneration becomes defective and accelerated causing the airway thickening. This condition has a very poor prognosis; on average patients survive only 2-3 years from diagnosis. Research at Salford investigates cellular ‘remodelling’ events in lung fibrosis and evaluates fibrosis reversal strategies. 2. During lung infections airways are characteristically infiltrated by large numbers of T lymphocytes that partly provide our protective immune responses. T lymphocytes have the ability to recognise and aid clearance of previously encountered infections, however, inflammation during the absence of infection (ie in Asthma and COPD) indicates altered adaptive immunity is contributing to the disease pathology.

近期论文

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Kaur, M & Smyth, D L & Cadden, P & Grundy, S & Ray, D & Plumb, J & Singh, D 2012, 'T lymphocyte insensitivity to corticosteroids in COPD', Respiratory Research, 13(20), pp.1-9. Eustace, A & Smyth, D L & Mitchell, L & Williamson, K & Plumb, J & Singh, D 2010, 'Identification of Interleukin-17 Producing Cells in the Lungs of COPD Patients.', Chest, 139, pp.1089 -1100. Smyth, L & Eustace, A & Kolsum, U & Blaikely, J & Singh, D 2010, 'Increased airway T regulatory cells in asthmatic subjects', Chest. Singh, D & Smyth, L & Borrill, Z & Sweeney, L & Tal-Singer, R 2010, 'A Randomised, Placebo Controlled Study Of The Effects Of The p38 MAPK Inhibitor SB-681323 On Blood Biomarkers Of Inflammation In COPD Patients', J Clin Pharmacol, 50, pp.94-100. Plumb, J & Smyth, L & Singh, D 2010, 'Role of regulatory T-cells in COPD', Annals of Res Med, 1, pp.45-52. Smyth, L & Eustace, A & Kolsum, U & Blaikely, J & Singh, D 2010, 'Response To Comment On Chest-10-1440: Increased Airway T Regulatory Cells In Asthmatic Subjects', Chest, 138, p.1283. Kent, L & Smyth, L & Plumb, J & Clayton, C & Fox, S & Ray, D & Farrow, S & Singh, D 2009, 'Inhibition of lipopolysaccharide-stimulated chronic obstructive pulmonary disease macrophage inflammatory gene expression by dexamethasone and the p38 mitogen-activated protein kinase inhibitor N-cyano-N'-(2-{[8-(2,6-difluorophenyl)-4-(4-fluoro-2-methylphenyl)-7-oxo-7,8-dihydropyrido[2,3-d] pyrimidin-2-yl]amino}ethyl)guanidine (SB706504).', Pharmacol Exp Ther, 328(2), pp.458-468. Plumb, J & Smyth, D L & Adams, H & Vestbo, J & Bentley, A & Singh, D 2009, 'Increased T-regulatory cells within lymphocyte follicles in moderate COPD.', Eur Respir J., 34(1), pp.89-94.

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