Professor David Greaves
Tutorial Fellow in Medicine
Professor of Inflammation Biology
David Greaves read Microbiology at Bristol and studied for a PhD in Biophysics and Molecular Biology at King’s College London (Winner of the Tadion-Rideal Medal). Postdoctoral research was undertaken at the Netherlands Cancer Institute in Amsterdam, the National Institute for Medical Research at Mill Hill in London and the Sir William Dunn School of Pathology in Oxford before being awarded a British Heart Foundation Basic Science Lectureship and subsequent election to a University Lectureship in Cell Pathology. In 2010 David Greaves was awarded the title of Professor of Inflammation Biology by the University of Oxford.
Find out more on his Faculty profile.
Undergraduate teaching
David Greaves leads the Hertford Medicine teaching team. Prof. Greaves tutors first year students for Biochemistry & Medical Genetics, Endocrinology and Cell Biology. He also tutors second year BM Principles of Pathology and third year modules in Cardiovascular Pathology and Innate Immunity.
Graduate teaching
Prof. Greaves is the Course Director of the Oxford 4-year Cardiovascular Sciences DPhil course, which awards four 4-year British Heart Foundation studentships a year. Prof. Greaves currently supervises three DPhil students in his laboratory.
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Research interests
Inflammation Biology – Acute Inflammation is the response of all tissues to injury and infection. Inflammation is characterised by the rapid recruitment of plasma proteins and white blood cells called neutrophils from the bloodstream. This process is usually short lived and is followed by a period of inflammation resolution when dead microbes, cell debris and dying host cells are removed by cells called macrophages.
Chronic inflammation is characterised by continuing inflammation and the build up of large numbers of macrophages and lymphocytes in diseased tissues such as the joints in rheumatoid arthritis. Work in the Greaves laboratory is aimed at understanding the key molecules that recruit and retain macrophages at sites of chronic inflammation and understanding the key pathways that initiate inflammation resolution.
Cardiovascular disease – Angina, heart attacks and ischaemic strokes are all caused by the same underlying disease process in arteries called atherosclerosis. Atherosclerosis is characterised by the build up of cholesterol containing lipoproteins and macrophages within the lining of major arteries.
Professor Greaves and collaborators within the Department of Cardiovascular Medicine are studying the molecular mechanisms that regulate the very earliest stages of atherosclerosis and investigating factors within atherosclerotic plaques that affect macrophage differentiation.In collaboration with Professor Ed Fisher at New York University we are examining models of atherosclerotic plaque regression with a special emphasis on how macrophage responses to chemokines can be modified by diabetes and hypertension.
Anti-inflammatory drug development – Recent work from the Greaves laboratory has shown that an FDA approved medicine called ibrutinib used for the treatment of a rare form of cancer has potent anti-diabetic and anti-inflammation effects that work by altering macrophage cell signalling. In current experiments we are exploring if this drug can have beneficial effects on macrophage cell biology in atherosclerosis.
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Publications
Selected recent papers from over 150 peer-reviewed articles:
- Cannabinoid receptor 2 deficiency exacerbates inflammation and neutrophil recruitment.
Theodore S. Kapellos, Lewis Taylor, Alexander Feuerborn, Sophia Valaris, Mohammed T. Hussain, G. E. Rainger, David R. Greaves and Asif J. Iqbal
Published Online:25 Feb 2019Â doi:10.1096/fj.201802524R. - Activation of the Immune-Metabolic Receptor GPR84 Enhances Inflammation and Phagocytosis in Macrophages.
Recio C, Lucy D, Purvis GSD, Iveson P, Zeboudj L, Iqbal AJ, Lin D, O’Callaghan C, Davison L, Griesbach E, Russell AJ, Wynne GM, Dib L, Monaco C, Greaves DR.
Front Immunol. 2018 Jun 20;9:1419. doi: 10.3389/fimmu.2018.01419. - In Vitro Migration Assays.
Taylor L, Recio C, Greaves DR, Iqbal AJ.
Methods Mol Biol. 2018;1784:197-214. doi: 10.1007/978-1-4939-7837-3_19. - Absence of the Non-Signalling Chemerin Receptor CCRL2 Exacerbates Acute Inflammatory Responses In Vivo.
Regan-Komito D, Valaris S, Kapellos TS, Recio C, Taylor L, Greaves DR, Iqbal AJ.
Front Immunol. 2017 Nov 21;8:1621. doi: 10.3389/fimmu.2017.01621. eCollection 2017. - The Role of Metabolite-Sensing G Protein-Coupled Receptors in Inflammation and Metabolic Disease.
Recio C, Lucy D, Iveson P, Iqbal AJ, Valaris S, Wynne G, Russell AJ, Choudhury RP, O’Callaghan C, Monaco C, Greaves DR.
Antioxid Redox Signal. 2018 Jul 20;29(3):237-256. doi: 10.1089/ars.2017.7168. - Tracking Monocyte Recruitment and Macrophage Accumulation in Atherosclerotic Plaque Progression Using a Novel hCD68GFP/ApoE-/- Reporter Mouse-Brief Report.
McNeill E, Iqbal AJ, Jones D, Patel J, Coutinho P, Taylor L, Greaves DR, Channon KM.
Arterioscler Thromb Vasc Biol. 2017 Feb;37(2):258-263. doi: 10.1161/ATVBAHA.116.308367. Epub 2016 Dec 1. - Inflammation-a Critical Appreciation of the Role of Myeloid Cells.
Iqbal AJ, Fisher EA, Greaves DR.
Microbiol Spectr. 2016 Oct;4(5). doi: 10.1128/microbiolspec.MCHD-0027-2016. Review. - Acute exposure to apolipoprotein A1 inhibits macrophage chemotaxis in vitro and monocyte recruitment in vivo.
Iqbal AJ, Barrett TJ, Taylor L, McNeill E, Manmadhan A, Recio C, Carmineri A, Brodermann MH, White GE, Cooper D, DiDonato JA, Zamanian-Daryoush M, Hazen SL, Channon KM, Greaves DR, Fisher EA.
Elife. 2016 Aug 30;5. pii: e15190. doi: 10.7554/eLife.15190. - Netrin-1 Reduces Monocyte and Macrophage Chemotaxis towards the Complement Component C5a.
Taylor L, Brodermann MH, McCaffary D, Iqbal AJ, Greaves DR.
PLoS One. 2016 Aug 10;11(8):e0160685. doi: 10.1371/journal.pone.0160685. - A novel real time imaging platform to quantify macrophage phagocytosis.
Kapellos TS, Taylor L, Lee H, Cowley SA, James WS, Iqbal AJ, Greaves DR.
Biochem Pharmacol. 2016 Sep 15;116:107-19. doi: 10.1016/j.bcp.2016.07.011. - Primary Macrophage Chemotaxis Induced by Cannabinoid Receptor 2 Agonists Occurs Independently of the CB2 Receptor.
Taylor L, Christou I, Kapellos TS, Buchan A, Brodermann MH, Gianella-Borradori M, Russell A, Iqbal AJ, Greaves DR.
Sci Rep. 2015 Jun 2;5:10682. doi: 10.1038/srep10682. - Ligand-based virtual screening identifies a family of selective cannabinoid receptor 2 agonists.
Gianella-Borradori M, Christou I, Bataille CJ, Cross RL, Wynne GM, Greaves DR, Russell AJ.
Bioorg Med Chem. 2015 Jan 1;23(1):241-63. doi: 10.1016/j.bmc.2014.11.002. - Fractalkine promotes human monocyte survival via a reduction in oxidative stress.
White GE, McNeill E, Channon KM, Greaves DR.
Arterioscler Thromb Vasc Biol. 2014 Dec;34(12):2554-62. doi: 10.1161/ATVBAHA.114.304717. - Human CD68 promoter GFP transgenic mice allow analysis of monocyte to macrophage differentiation in vivo.
Iqbal AJ, McNeill E, Kapellos TS, Regan-Komito D, Norman S, Burd S, Smart N, Machemer DE, Stylianou E, McShane H, Channon KM, Chawla A, Greaves DR.
Blood. 2014 Oct 9;124(15):e33-44. doi: 10.1182/blood-2014-04-568691. - A real time chemotaxis assay unveils unique migratory profiles amongst different primary murine macrophages.
Iqbal AJ, Regan-Komito D, Christou I, White GE, McNeill E, Kenyon A, Taylor L, Kapellos TS, Fisher EA, Channon KM, Greaves DR.
PLoS One. 2013;8(3):e58744. doi: 10.1371/journal.pone.0058744. - CC chemokine receptors and chronic inflammation–therapeutic opportunities and pharmacological challenges.
White GE, Iqbal AJ, Greaves DR.
Pharmacol Rev. 2013 Jan 8;65(1):47-89. doi: 10.1124/pr.111.005074. Print 2013 Jan. Review. - Macrophage differentiation and function in atherosclerosis: opportunities for therapeutic intervention?
Williams HJ, Fisher EA, Greaves DR.
J Innate Immun. 2012;4(5-6):498-508. doi: 10.1159/000336618. Epub 2012 Apr 27. Review.
- Cannabinoid receptor 2 deficiency exacerbates inflammation and neutrophil recruitment.