Prof Philip Taylor
Professor of Translational Immunology, Cardiff Institute of Infection & Immunity
Research overview
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.
Research description
Selected Projects
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 - 31.07.2012
Value: Award pending confirmation
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 beta glucan receptor Dectin-1, in the regulation of inflammatory cell recruitment and cellular activation during inflammation.
- to develop novel models for the study of myeloid cells (particularly macrophages) during health and disease.
Keywords: Macrophage, Inflammation, Fungi, Dectin-1, mouse-models.
Project Name: Conditional-immortalisation of granulocyte precursors to model innate immune responses.
Funder: I3-IRG (School of Medicine) and the Medical Research Council.
Duration: 2007-2010
Value: Approx £75,000
Background/Introduction: Myeloid cells such as macrophages and granulocytes 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) are thought to play an important role in fungal recognition and cellular activation.
We have found that Dectin-1 plays an important role in cellular activation during fungal infection. Dectin-1 is expressed by many myeloid cell subsets and has distinct isoforms expressed in a cell specific manner. The ability to study the role of myeloid cells in vitro is often hampered by their short life spans, lack of amenability to genetic manipulation and the difficulties involved in isolating them in quiescent states.
Aims: The aim of this studentship is to develop novel models to study the regulation of the expression and function of Dectin-1 in myeloid cell subsets in vitro.
Keywords: Granulocytes, Dectin-1, Innate immunity, Fungi, in vitro.
Project Name: Regulation of myeloid cells in innate immune inflammation.
Funder: The Wellcome Trust (Research Career Development Fellowship).
Duration: 01.08.2003 - 31.07.2007
Value: £481,748
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.
Aims: The primary aim of this fellowship is to characterise the role of select Pattern Recognition Receptors, such as Dectin-1, in the regulation of inflammatory cell recruitment and cellular activation after fungal infection
Keywords: Macrophage, Inflammation, Fungi, Dectin-1, mouse-models.
Career Profile
- 2007-2012
Medical Research Council Senior Non-Clinical Fellowship
(Cardiff University School of Medicine, Cardiff, UK)
- 2003-2007
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)
- 1999-2003
Wellcome Trust postdoctoral research assistant
(Sir William Dunn School of Pathology, Oxford University, UK)
- 1998-1999
Wellcome Trust postdoctoral research assistant
(Hammersmith Hospital, Imperial College School of Medicine, London, UK)
- 1997-1998
Arthritis Research Campaign postdoctoral research assistant
(Hammersmith Hospital, Imperial College School of Medicine, London, UK)
- 1994-1997
Medical Research Council PhD studentship
(Hammersmith Hospital, Imperial College School of Medicine, London, UK).
Awards and Prizes
- Medical Research Council Senior Non-Clinical Fellowship, 2007-2012
- Wellcome Trust Research Career Development Fellowship in Basic Biomedical Science, 2003-2007
- Medical Research Council PhD studentship, 1994-1997.
Memberships/External Activities
- 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
- Keystone Symposia Innate Immunity 2006. 10-15/02/2006. Banff, Alberta, Canada.
- British Society of Immunology Congress 2005. 06-09/12/2005. Harrogate International Centre, UK.
- British Society of Immunology Congress 2004. 07-10/12/2004. Harrogate International Centre, UK
Teaching Profile
- Miss Samantha Griffiths (DPhil Student): Day to day supervision (shared) 2003-2007 (Oxford University)
- Miss Sigrid Heinsbroek (DPhil Student): Cosupervisor (Completed November, 2005) (Oxford University)
- Lectures for FHS Immunity and Infection, Oxford University, 2003
- Revision seminars for FHS Immunity and Infection, Oxford University, 2003
- Tutorials for FHS Immunity and Infection, Oxford University, 2003.
Selected key publications
- Dectin-2 is a Syk-coupled pattern recognition receptor crucial for Th17 responses to fungal infection.
Robinson MJ, Osorio F, Rosas M, Freitas RP, Schweighoffer E, Gross O, Verbeek JS, Ruland J, Tybulewicz V, Brown GD, Moita LF, Taylor PR, Reis e Sousa C, J Exp Med, Volume 206, 9 (August 2009) pp.2037-2051 - Dectin-1 is required for beta-glucan recognition and control of fungal infection.
Taylor PR, Tsoni SV, Willment JA, Dennehy KM, Rosas M, Findon H, Haynes K, Steele C, Botto M, Gordon S, Brown GD, Nat Immunol, Volume 8, 1 (January 2007) pp.31-38 - Monocyte and macrophage heterogeneity.
Gordon S, Taylor PR, Nat Rev Immunol, Volume 5, 12 (December 2005) pp.953-964 - The beta-glucan receptor, dectin-1, is predominantly expressed on the surface of cells of the monocyte/macrophage and neutrophil lineages.
Taylor PR, Brown GD, Reid DM, Willment JA, Martinez-Pomares L, Gordon S, Wong SY, J Immunol, Volume 169, 7 (October 2002) pp.3876-3882 - Dectin-1 is a major beta-glucan receptor on macrophages.
Brown GD, Taylor PR, Reid DM, Willment JA, Williams DL, Martinez-Pomares L, Wong SY, Gordon S, J Exp Med, Volume 196, 3 (August 2002) pp.407-412 - A hierarchical role for classical pathway complement proteins in the clearance of apoptotic cells in vivo.
Taylor PR, Carugati A, Fadok VA, Cook HT, Andrews M, Carroll MC, Savill JS, Henson PM, Botto M, Walport MJ, J Exp Med, Volume 192, 3 (August 2000) pp.359-366
