Prof Philip Taylor
Professor of Translational Immunology, Division of Infection & Immunity
I began my research career with a PhD in the laboratory of Prof. Mark Walport (Imperial College School of Medicine, London) on the generation and study of complement-deficient mice. During this time, and the subsequent two years of post-doctoral research under the supervision of both Prof. Walport and Prof. Marina Botto, I obtained extensive experience in the study of innate immunity, inflammation and aspects of infection and autoimmunity.
Subsequently I took a post-doctoral position in the laboratory of Prof. Siamon Gordon (Sir William Dunn School of Pathology, Oxford). I acquired an interest in macrophage biology and the cell surface receptors involved in microbial recognition. From this interest and my initial studies of the leukocyte beta-glucan receptor (Dectin-1) I was awarded (2003) a Wellcome Trust Research Career Development Fellowship (RCDF) in Basic Biomedical Science (Sponsored by Prof. Gordon). The RCDF allowed me to establish and run my own laboratory and further develop my interest in myeloid cell activation during inflammation.
More recently, I transferred my Wellcome Trust RCDF to Cardiff University’s School of Medicine (2006; Sponsored by Prof. B. Paul Morgan). I have just (2007) been awarded a Medical Research Council Senior Non-Clinical Fellowship to continue the study of myeloid cells during inflammation. This will involve a particular emphasis on the physiological role of Dectin-1, but also on the development of new models to facilitate this type of research.
See the Myeloid Cell Biology Group
Education & Qualifications
1998: PhD, Molecular Genetics, Imperial College London.
1994: B.Sc, Human Genetics, University College London.
Project Name: Defining the role of peritoneal dendritic cells in tissue specific immunity and the clinical application of peritoneal dialysis.
Funder: The Medical Research Council.
Duration: 01.08.20013 - 31.07.2016
Value: ~£570K (fEC)
Background/Introduction: Worldwide, >240,000 individuals rely on peritoneal dialysis (PD) for treatment of renal failure. In countries with developing economies this figure grows by 30% each year. However, only a third of PD patients manage to continue therapy beyond 3 years. This is in part due to an unacceptably high mortality rate (25%) for end-stage renal failure patients, and compounding technique failures (23%) which preclude the long-term use of PD as a clinical therapy. The main contributing factors to this problem are peritoneal infection, and inflammation-driven fibrosis that leads to peritoneal membrane failure and, in a minority of cases, a severe encapsulating peritoneal sclerosis. Development of fibrosis is linked to treatment duration, and repeated incidence of bacterial peritonitis and the development of an adaptive immune response.
Aims: The aims of the project are:
- To functionallycharacterise the newly-identified peritoneal dendritic cells found in PDpatients and mice.
- To determine themechanism of dendritic cell recruitment and retention in a reverse translatedmouse model of peritoneal fibrosis caused by multiple inflammatory episodes.
- To determine therole of peritoneal dendritic cell in initiation and resolution of inflammatoryepisodes.
- To determine ifthe accumulation of dendritic cell populations in the peritoneal cavity ofdialysis patients has prognostic value with regard to membrane damage.
Project Name: Targeting tissue macrophage generation as a mechanism to modulate the resolution of inflammation.
Funder: The Medical Research Council.
Duration: 01.08.2012 - 31.07.2015
Value: ~£580K (fEC)
Background/Introduction: It is often assumed that macrophages are a heterogeneous mix of cells with broadly similar roles in homeostatic control, host defence and immunity, the resolution of inflammation and wound repair. However, contemporary evidence identifies that macrophages are in reality derived from distinct lineages with defined specific in vivo functions. Myeloid cells such as macrophages express cell surface receptors for the recognition of microbes. These receptors play a role in the activation of the cells and the development of the subsequent inflammatory response. We intend to define novel inflammatory pathways or processes in macrophages that effect the balance between the beneficial effects of resolving inflammation and the need for competent host defence whilst minimising tissue damage. We propose to achieve this by selectively manipulating the existence, renewal and/or phenotype of tissue resident macrophgaes in vivo. To investigate these events, studies will focus on the impact of tissue macrophage development, turnover and effector function during homeostasis, acute resolving inflammation and repeated inflammation leading to tissue damage.
Aims: The aims of the project are:
- To establish theregulatory mechanisms involved in tissue macrophage that balance theirnon-proliferative quiescent state with one of active proliferation.
- To establish theroles of select transcription factors in the maturation andproliferative/non-proliferative/quiescent and immune phenotypes of tissuemacrophages.
- To specificallymanipulate tissue macrophage phenotype to establish the impact of selecttranscription factor expression on tissue macrophage immune functions effectivehost defence and resolution of inflammation whilst minimising tissue damage.
Project Name: Pattern recognition receptors and the recruitment and differentiation of myeloid cells in inflammation.
Funder: The Medical Research Council (Senior Non-Clinical Fellowship).
Duration: 01.08.2007 - 31.07.2014
Value: ~£1.6M (fEC).
Background/Introduction: Myeloid cells such as macrophages express cell surface receptors for the recognition of microbes. These receptors play a role in the activation of the cells and the development of the subsequent inflammatory response. In the context of fungal infection lectins, such as the leukocyte beta glucan receptor (Dectin-1) and mannose receptors such as members of the DC-SIGN family and the macrophage mannose receptor, are thought to play an important role in fungal recognition and cellular activation.
We have demonstrated that Dectin-1 plays an important role in the induction of the anti-fungal inflammatory response in vivo. Deficiency of Dectin-1 results in impaired host defence and increased susceptibility to fungal infections. The consequence of myeloid cell activation by specific ligation of Dectin-1 during fungal infection is poorly understood and in vivo models for the study of cellular systems such as these have lagged behind those of other immune cells.
Aims: The aims of the fellowship are:
- to characterise the role of the leukocyte betaglucan receptor Dectin-1, in the regulation of inflammatory cell recruitmentand cellular activation during inflammation.
- to develop novel models for the study of myeloidcells (particularly macrophages) during health and disease.
Keywords: Macrophage, Inflammation, Fungi, Dectin-1, mouse-models.
Professor of Translational Immunology (Cardiff University School of Medicine, Cardiff, UK).
Medical Research Council Senior Non-Clinical Fellowship (Cardiff University School of Medicine, Cardiff, UK).
Wellcome Trust Research Career Development Fellowship in Basic Biomedical Science (Sir William Dunn School of Pathology, Oxford University, UK; and transferred to Cardiff University School of Medicine, Cardiff, UK).
Wellcome Trust postdoctoral research assistant (Sir William Dunn School of Pathology, Oxford University, UK).
Wellcome Trust postdoctoral research assistant (Hammersmith Hospital, Imperial College School of Medicine, London, UK).
Arthritis Research Campaign postdoctoral research assistant (Hammersmith Hospital, Imperial College School of Medicine, London, UK).
Medical Research Council PhD studentship (Hammersmith Hospital, Imperial College School of Medicine, London, UK).
Awards and Prizes
- Medical Research Council Senior Non-ClinicalFellowship, 2007-2012.
- Wellcome Trust Research Career DevelopmentFellowship in Basic Biomedical Science, 2003-2007.
- Medical Research Council PhD studentship,1994-1997.
- Editorial Board Member for Clinical and Experimental Immunology.
- Editor for Frontiers in Antigen Presenting Cell Biology.
- Member of the British Society of Immunology.
- Member of the Research Defence Society.
- Member of the steering committee of the Infection, Immunity and Inflammation interdisciplinary research group (i3-IRG) within the Cardiff University's School of Medicine.
Conference presentations and invited seminars
- Department of Infection and Immunity, SheffieldUniversity Medical School, UK. 10/07/13.
- Department of Pathology, Cambridge, UK. 12/06/13.
- Institutefor Systemic Inflammation Research “DistinguishedLecturer Series”, University of Lübeck, Germany, 24/4/2013.
- University College London, 6/12/2012.
- British Society of Medical Microbiology AnnualMeeting, Cardiff. 1-3/5/2012.
- Bristol Immunology Group “Autoimmunity andAutoinflammation” day, Bristol. 12/03/2012.
- MRC Mammalian Genetics Unit, Harwell, Oxfordshire.22/11/2011.
- Division of Medicine, Hammersmith Hospital, ImperialCollege London. 04/11/2011.
- Cambridge University Sackler Seminar Series.19/11/2010.
- Babraham Institute, Cambridge. 27/10/2009.
- British Society of Immunology Summer School 2009.17/07/2009. Bristol, UK
- Trinity College Dublin. 07/05/2009.
- British Society of Immunology Congress 2008.17-21/11/2008. SECC, Glasgow, UK.
- INSERMworkshop on "Toll-like receptors" in October 2008. Toulon, France.
- Department of Microbiology and Immunology, GöteborgUniversity, Gothenburg, Sweden.
- KeystoneSymposia Innate Immunity 2006. 10-15/02/2006. Banff, Alberta, Canada.
- Instituteof Immunology and Infection Research, Edinburgh University. 19/12/2005.
- BritishSociety of Immunology Congress 2005. 06-09/12/2005. Harrogate, UK.
- Department ofInfection and Immunity Unit, York University. 30/11/2005.
- Department ofMedical Biochemistry and Immunology, Cardiff University. 28/09/2005.
- BritishSociety of Immunology Congress 2004. 07-10/12/2004. Harrogate, UK.
- King’s College London. 25/11/2003.
- Division of Medicine, Hammersmith Hospital, ImperialCollege London. 14/11/2003.
PhD/DPhil Student Training
- Mr. Robert Pickering: Primary Supervisor(2013-2016) (Cardiff University).
- Miss Leah Wallace: Primary Supervisor (2013-2016)(Cardiff University).
- Miss Christine Hinz: Cosupervisor (2013-2016)(Cardiff University).
- Miss Melisa Lopez Anton: Cosupervisor (2012-2015)(Cardiff University).
- Dr. Chia-Te Liao: Primary Supervisor (2011-2014)(Cardiff University).
- Mr. Luke Davies: Primary Supervisor (2010-2014)(CardiffUniversity).
- Mr. Christopher Rice: Cosupervisor (2010-2013)(CardiffUniversity).
- Miss Ravinder Singh: Cosupervisor(2009-2013)(Cardiff University).
- Miss Jacqueline McDonald: Primary supervisor(completed 2013) (Cardiff University).
- Miss Samantha Griffiths: Cosupervisor (completed 2007)(Oxford University).
- Miss Sigrid Heinsbroek: Cosupervisor (Completed2005) (Oxford University).
- Teaching on Cardiff University’s C21 Medicine programme.
- Teaching on Medical School Student SelectedComponents (Cardiff University, 2007-present).
- Lectures for FHS Immunity and Infection, OxfordUniversity, 2003.
- Revision seminars for FHS Immunity and Infection,Oxford University, 2003.
- Tutorials for FHS Immunity and Infection, OxfordUniversity, 2003.
Recent key publications
- Distinct bone marrow-derived and tissue-resident macrophage lineages proliferate at key stages during inflammation. Nat Commun, Volume 4 2013 p. 1886
- Anti-inflammatory activity of IgG1 mediated by Fc galactosylation and association of FcγRIIB and dectin-1. Nat Med, Volume 18, 9 September 2012 pp.1401-1406
- Dectin-2 is a Syk-coupled pattern recognition receptor crucial for Th17 responses to fungal infection. J Exp Med, Volume 206, 9 August 2009 pp.2037-2051
- Dectin-1 is required for beta-glucan recognition and control of fungal infection. Nat Immunol, Volume 8, 1 January 2007 pp.31-38
- Monocyte and macrophage heterogeneity. Nat Rev Immunol, Volume 5, 12 December 2005 pp.953-964
- Dectin-1 is a major beta-glucan receptor on macrophages. J Exp Med, Volume 196, 3 August 2002 pp.407-412