Immunology research within the Institute incorporates cytokine and chemokine biology, immune cell signalling, advanced imaging technologies, and cellular and gut immunology. Our translational efforts are focused on rheumatoid arthritis, dermatology, respiratory and central nervous system immune and inflammatory diseases.
PhD Research Projects
Project Title: Cytokine biology and disease pathogenesis
Supervisor: Prof Iain B McInnes
- Project outline:Unravelling the mechanisms of inflammation within the damaged joint in patients with rheumatoid arthritis has lead to the development of new therapeutics and in consequence has revolutionized the management of this and related inflammatory diseases. Our group has an internationally recognised track record in examining those molecular events that regulate chronic inflammation in people with rheumatoid and psoriatic arthritis. Projects contained in our group examine the molecular and cellular regulation of cytokine production and particularly how such expression can be perpetuated in the context of innate to adaptive immune transition. We further more offer opportunity to study the role of microRNA in such processes. The laboratory science is closely linked to the translational science that is performed in the ARUK Centre of Excellence for investigation of rheumatoid arthritis pathogenesis.
- Summary aim:To explore novel pathways regulating cytokine expression in rheumatoid and related inflammatory arthritis. To thereby learn about the detailed biology of novel cytokines and their effector functions. Finally to understand how such knowledge can inform new therapeutics.
- Techniques to be used: RT-PCR, sequencing, miR technologies, cell purification and culture (primary and secondary), FACS, luminex, in vivo inflammatory models
- References:1. McInnes IB, Kavanaugh A, Gottlieb AB, Puig L, Rahman P, Ritchlin C, Brodmerkel C, Li S, Wang Y, Mendelsohn AM, Doyle MK. Efficacy and safety of the anti-IL-12/23 p40 monoclonal antibody ustekinumab in patients with active psoriatic arthritis despite conventional therapy: 1 year results of the phase 3, multicentre, double–blind, placebo controlled PSUMMIT 1 trial. Lancet 2013 (In press)
2. McInnes IB, Schett G. The pathogenesis of rheumatoid arthritis. N Engl J Med. 2011 Dec 8-362(23):2205-19. Review. PMID 22150039
3. McInnes IB, Schett G. Cytokines in the pathogenesis of rheumatoid arthritis Nature Rev Immunol 2007 Jun;7(6):429-429 PMID: 17525752
- Contact: Prof Iain B McInnes (firstname.lastname@example.org) FRCP, PhD, FRSE, FMedSci; Muirhead Professor of Medicine & Director, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences,University of Glasgow,120 University Place,Glasgow, G12 8TA
Project Title: T cell/APC interactions and immunological decisions
Supervisor: Prof James Brewer & Prof Paul Garside
- Project outline:It is becoming clear that the duration, frequency, and intensity of T cell/APC interactions, determines the induction of immunological tolerance versus priming. However, the detailed molecular mechanisms regulating cellular interactions in vivo remain unclear. We contend that spatiotemporal context has a critical influence on T/APC interactions and consequently the induction, maintenance and/or control of immune responses. For example, we have recently shown that the duration and magnitude antigen presentation and the subsequent T cell/APC interaction can influence differentiation of T cells to the Tfh phenotype responsible for driving B cell antibody production. Consequently, cellular and molecular interactions must be carefully choreographed in space and time to provide normal immune function giving protection against infection while avoiding autoimmunity. On the other hand, dysregulated spatiotemporal expression of molecules involved in T cell/APC interactions may result in pathology.
- Summary aim: 1. What are the molecular mechanisms controlling T/APC interactions during priming and tolerance in vivo?
2. How do these pathways impact on the duration, frequency and intensity of T cell/APC interactions in Lymph Nodes (LN)?
- Techniques to be used: High content (INCELL) imaging, Live in vitro microscope, Intravital multiphoton microscopy
- References: 1. Zinselmeyer, B. H. et al. In situ characterization of CD4+ T cell behavior in mucosal and systemic lymphoid tissues during the induction of oral priming and tolerance. J. Exp. Med. 201, 1815–23 (2005).
2. Millington, O. R. et al. Malaria impairs T cell clustering and immune priming despite normal signal 1 from dendritic cells. PLoS pathogens 3, 1380–7 (2007).
3. Celli, S., Lemaître, F. & Bousso, P. Real-time manipulation of T cell-dendritic cell interactions in vivo reveals the importance of prolonged contacts for CD4+ T cell activation. Immunity 27, 625–34 (2007).
- Contact: email@example.com; firstname.lastname@example.org
Project Title: Investigating genetic and microenvironmental drivers of central nervous system metastasis in childhood acute lymphoblastic leukaemia.
Supervisor: Dr Christina Halsey
- Project outline:Despite recent advances in childhood acute lymphoblastic leukaemia (ALL) therapy, challenges remain. Little is known about risk-factors and biology of central nervous system (CNS) infiltration by leukaemic blasts1. Therefore, all children receive potentially toxic CNS-directed therapy and some children suffer from refractory CNS disease incurable with current approaches. In this project we aim to identify key phenotypic differences between CNS and bone marrow (BM) leukaemic blasts and look for genetic and environmental drivers of CNS relapse. We have established a xenograft model of leukaemic infiltration of the CNS. Using this model the degree of CNS tropism will be investigated using serial transplantation of cells retrieved from the CNS compartment. Dynamic engraftment will be visualised using bioluminescent imaging (IVIS spectrum)2. Cells will also be retrieved from the CNS and BM compartments and examined for transcriptional differences using RNA-sequencing and clonal differences using multicolour FISH3. These investigations will be complemented by an in vitro model of blast-stromal interactions in order to investigate microenvironmental versus cell-intrinsic differences and to test candidate genes and pathways identified by transcriptomics. As well as providing essential biological insight into mechanisms of CNS disease this project has the potential to improve risk-stratification of CNS-directed treatment, aid the evaluation of new drugs and identify therapeutic targets for resistant disease.
- Summary aim:To determine the relative roles of genetic versus environmental factors in determining the risk of CNS relapse of leukaemia.
- Techniques to be used:In vivo xenograft model of primary ALL engraftment using immunodeficient NOD.Cg-PrkdcscidIl2rgtm1Wjl/SzJ (NSG) mice, IVIS imaging, Cell culture, apoptosis, cell cycle and viability assays, Gene knockdown, RNA-sequencing
- References:1. Pui CH, Howard SC. Current management and challenges of malignant disease in the CNS in paediatric leukaemia. Lancet Oncol. 2008;9(3):257-268.
2. Bomken S, Buechler L, Rehe K, et al. Lentiviral marking of patient-derived acute lymphoblastic leukaemic cells allows in vivo tracking of disease progression. Leukemia. 2013;27(3):718-721.
3. Anderson K, Lutz C, van Delft FW, et al. Genetic variegation of clonal architecture and propagating cells in leukaemia. Nature. 2011;469(7330):356-361.
- Contact:Dr Christina Halsey (email@example.com), Level 3, Glasgow Biomedical Research Centre, Institute of Infection, Immunity and Inflammation,College of MVLS University of Glasgow, 120, University Place, Glasgow G12 8TA
Project Title: IRegulation of Inflammation by NF-κB ubiquitination
Supervisor: Dr. Ruaidhrí Carmody
- Project outline:NF-κB is the master regulator of the immune response and is essential for the development and homeostasis of the immune system. It is an essential mediator of inflammatory responses and plays a central role in chronic inflammatory diseases including arthritis, inflammatory bowel disease and autoimmunity. The ubiquitination and proteasomal degradation of NF-κB in the nucleus is a critical mechanism for the termination of NF-κB transcriptional activity and is a major regulatory factor in the expression of pro-inflammatory genes [1,2]. The ubiquitination of NF-κB is dependent on DNA binding and may be modulated by phosphorylation at specific sites. The NF-κB deubiquitinase, USP7, is essential for NF-κB transcriptional activity and it’s inhibition results in the blockade of Toll-like receptor induced pro-inflammatory cytokine gene expression . This project will identify key regulatory events which control the deubiquitination of NF-κB by USP7, including site specific phosphorylation. Furthermore, this project will investigate the role of USP7 mediated deubiquitination of NF-κB in promoting inflammation in established mouse models of peritonitis, arthritis and dermatitis. The data from these experiments will not only deepen our understanding of the regulation of NF-κB but will also assess the potential impact of small molecule inhibitors of USP7 on inflammatory disease.
- Summary aim:This project will investigate the role of NF-κB deubiquitination by USP7 in the regulation of inflammation.
- Techniques to be used:cell culture, real-time PCR, chromatin immunoprecipitation, molecular biology (including site directed mutagenesis), immunoblotting, in vivo models of inflammation (e.g. zymosan induced peritonitis, antibody-induced arthritis, dermatitis).
- References:1. Carmody RJ, Ruan Q, Hilliard B, Palmer S, Chen YH (2007) Negative regulation of Toll-Like Receptor Signaling by NF-?B p50 Ubiquitination Blockade. Science 317:675-678.
2. Yan Q, Carmody RJ, Qu Z, Ruan Q, Jager J, Mullican SE, Lazar MA, Chen YH. (2012) Nuclear factor-κB binding motifs specify Toll-like receptor-induced gene repression through an inducible repressosome. Proceedings Of the National Academy of Sciences USA 28;109(35):14140-5
3. Colleran A, Collins PE, O'Carroll C, Ahmed A, Mao X, McManus B, Kiely PA, Burstein E, Carmody RJ. (2013) De-ubiquitination of NF-κB by Ubiquitin-Specific Protease-7 Promotes Transcription. Proceedings Of the National Academy of Sciences USA. 110(2):618-23.
- Contact:Ruaidhrí Carmody (firstname.lastname@example.org), Sir Graeme Davies Building, Institute of Infection, Immunity and Inflammation, University of Glasgow, Room B/316, 120 University Place, Glasgow, G12 8TA Tel: 0141 330 5945
Project Title: Impact of virus infection on dendritic cell function and migration to draining lymph nodes.
Supervisor: Dr Clive McKimmie
- Project outline:Globalisation and climate change are facilitating an increase in the incidence of infectious disease, including those that affect economically important livestock. This includes infections caused by viruses that are spread by biting insects, known as arboviruses. Arboviruses replicate to exceptionally high levels in the blood, so that the probability of their progeny being sampled by a second feeding insect is sufficiently high for animal-to-animal spread to occur. The route by which arboviruses spread from the mosquito bite site in the skin to blood is a critical stage of the virus life cycle that is poorly understood. This project will investigate whether spread of virus from mosquito bites is facilitated by the migration of leukocytes, such as Dendritic cells (DC), from skin to draining lymph nodes. DC act as sentinels to infection and migrate from the skin to draining lymph nodes. These cells have been shown to be the target of infection by some arboviruses. However, it is not clear whether infection of skin DC; (i) suppresses adaptive immune activation or (ii) facilitates dissemination to lymph nodes in migrating cells. Recent work in our group has determined that arboviruses infect DCs. The objectives of this project will be to determine the in vivo relevance of these findings.
- Summary aim:This project is an inter-disciplinary proposal that combines three related but rarely connected areas of research; in vivo immunobiology, molecular virology and arthropod vector biology. The project will gain fundamental knowledge on arthropod-mammalian interactions and how these processes affect the early stages of arthropod-borne virus (arbovirus) infection of mammals. Europe, once confident in its isolation from substantial arbovirus epidemics is now at risk, as witnessed by the recent outbreaks of viruses such as Bluetongue and Schmallenberg, which infect economically important ruminants. Understanding the mechanisms by which arboviruses infects mammals, disseminates in the host and causes disease, will enable us to identify the most relevant aspects for disease control and prevention. One area that is not well understood is how arboviruses initially establish infection in their mammalian host, following transfer from the arthropod vector. The project will combine expertise from across the institute, to utilize both molecular and cellular approaches to define the relevance of DC infection by arboviruses and so characterize a fundamental and important aspect of arthropod-mammal-virus biology.
- Techniques to be used: This project will use a variety of techniques that include flow cytometry, quantitative PCR and microscopy to determine extent of DC infection in vivo and the impact this has on DC function and viability.
- References:1. Jones, K. E. et al. Global trends in emerging infectious diseases. Nature 451, 990–993 (2008).
2. Shabman, R. S. et al. Journal of Virology 81, 237–247 (2006)
3. Gardner, C. L. et al. Journal of Virology 82, 10634–10646 (2008)
- Contact: Clive McKimmie (email@example.com) PhD, Lord Kelvin Adam Smith Research Fellow, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, B310 Sir Graeme Davies Building, University of Glasgow, 120 University Place, G12 8TA, +44 (0)141 330 2082,
Group website: www.chemokineresearchgroup.org
Project Title: The role of microRNA-34a in myeloid cells biology with relevance to the onset and progression of Arthritis
Supervisor: Dr Mariola Kurowska-Stolarska
- Project outline:The development of new treatments for rheumatoid arthritis (RA) is limited by our incomplete understanding of disease pathogenesis. Particularly, those pathways mediating disease onset, failed repair, and the development of treatment-refractory states are poorly understood. Myeloid cells (including dendritic cells, monocytes, macrophages) likely participate in such processes in RA. We recently discovered a novel epigenetic control mechanism of myeloid cells mediated via microRNA-34a and obtained evidence for deregulation of this process in RA.
- Summary aim:The aim of the project is to investigate how microRNA-34a regulates the basic biology of myeloid cells and thereafter elaborate new understanding of the role of microRNA-34a in experimental and clinical arthritis models.
- Techniques to be used: We have generated sponge technology to precisely manipulate microRNA-34a expression in vitro and technology to construct mice expressing these microRNA-34a specific inhibitors under monocyte/macrophage or dendritic cell promoters to achieve cell-type specific inhibition in vivo. We will access RA tissues in distinct disease stages, states, and therapeutics within our recently established RA Centre of Excellence to directly determine the impact of microRNA-34a inhibition ex vivo in pathologic cell lineages. qPCR, cell culture, primary cell transfections, FACS, Elisa, Western blot, luciferase assays will be used.
- References:1. MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis.Kurowska-Stolarska M et al., Proc Natl Acad Sci U S A. 2011,108(27):11193-8.
2. Cutting edge: miR-223 and EBV miR-BART15 regulate the NLRP3 inflammasome and IL-1β production. Haneklaus M et al.,J Immunol. 2012, 15;189(8):3795-9.
- Contact: Mariola.Kurowska-Stolarska@glasgow.ac.uk; Msks1y@clinmed.gla.ac.uk
Project Title: Investigating Immune Response in Experimental Atherosclerosis
Supervisor: Dr Pasquale Maffia
- Project outline:Immune responses play a key role in atherosclerosis1. The aim of this project is to combine our expertise of tracking immune response with the use of well established murine models of atherosclerosis in order to study the net contribution of specific cell subsets (in particular T follicular helper cells and plasmacytoid dendritic cells2) to atherosclerotic immune response.
- Techniques to be used:The project will provide training in both vascular biology and immunology, including flow cytometry, histology and microscopy3.
- References:1. Galkina E, Ley K. Immune and inflammatory mechanisms of atherosclerosis. Annu Rev Immunol. 2009;27:165-97.
2. Grassia G, MacRitchie N, Platt AM, Brewer JM, Garside P, Maffia P. Plasmacytoid dendritic cells: biomarkers or potential therapeutic targets in atherosclerosis? Pharmacol Ther. 2013;137:172-82.
3. Macritchie N, Grassia G, Sabir SR, Maddaluno M, Welsh P, Sattar N, Ialenti A, Kurowska-Stolarska M, McInnes IB, Brewer JM, Garside P, Maffia P. Plasmacytoid dendritic cells play a key role in promoting atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol. 2012 ;32:2569-79.
- Contact: Pasquale Maffia (Pasquale.Maffia@glasgow.ac.uk), Senior Lecturer, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Sir Graeme Davies Building, 120 University Place, Glasgow G12 8TA
Project Title: Heparin sulphates in the repair of the damaged CNS
Supervisor: Prof Susan C Barnett
- Project outline:CNS damage results in loss of nerves and their insulating myelin sheath, as well as an immediate immunological response which can influence repair in either a negative and positive manner. In addition major glial cells, termed astrocytes become activated. Astroglyosis is a hallmark of disease and results in inability of nerves to repair due to the formation of a gliotic scar. We have recently shown that heparan sulpate proteoglycans (HSPGs), depending on their sulphation levels can have varying affects on astroglyosis. Preliminary data suggest nerve outgrowth and myelination can also be influenced. Various in vitro cultures are being used to identify mechanism of this effect and identify novel strategies for CNS repair. We also have projects to study the effect of chemokines on myelination and astroglyosis and continue to identify novel strategies for the repair of the damaged CNS.
- Summary aim:To identify novel strategies for CNS repair and focus on nerve outgrowth, myelination and reduction in astroglyosis.
- Techniques to be used:Complex differentiating neural cell cultures, neural/mesenchymal stem cell types, immunefluorescence, fluorescent/confocal microscopy, RT-PCR, Western Blots, miR technologies, cell purification and various models of CNS injury in culture.
- References:1. Higginson JR, Thompson SM, Santos-Silva A, Guimond SE, Turnbull JE, Barnett SC. (2012) Differential sulfation remodelling of heparan sulfate by extracellular 6-O-sulfatases regulates fibroblast growth factor-induced boundary formation by glial cells: implications for glial cell transplantation. J Neurosci. 32(45):15902-12.
2. Barnett SC, Linington C. (2013) Myelination: do astrocytes play a role? Neuroscientist. 19(5):442-50.
3. Boomkamp SD, Riehle MO, Wood J, Olson MF, Barnett SC. (2012) The development of a rat in vitro model of spinal cord injury demonstrating the additive effects of Rho and ROCK inhibitors on neurite outgrowth and myelination. Glia. 60(3):441-56.
- Contact: Prof Sue C Barnett (Susan.Barnett@glasgow.ac.uk), PhD FSB, Professor of Cellular Neuroscience, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, 120 University Place, Glasgow, G12 8TA
Project Title: Cross-talk between immune and growth factor mediated responses in progressive multiple sclerosis.
Supervisor: Professor Chris Linington
- Project outline:Accumulation of disability in progressive forms of multiple sclerosis is attributed to a chronic inflammatory response sequestered within the central nervous system, but the mechanisms involved remain unknown1,2. Recent data obtained in this laboratory identify signal transduction by fibroblast growth factor (FGF9) as a mechanism that contributes to this chronic inflammatory response by generating a pro-inflammatory environment in which remyelination is inhibited; a combination of effects predicted to exacerbate axonal injury and loss3. We have identified increased expression of chemokines and TNF-associated effector pathways, extracellular matrix remodelling and dysregulation of insulin-like growth factor and IL6/gp130 cytokine signalling as factors that contribute to these effects in vitro, but it is now imperative to validate these findings in patients.
- Summary aim:This project will use matrix-assisted laser desorption ionization (MALDI)-based imaging mass spectrometry (IMS)4 to define the role of FGF mediated signal transduction in lesion formation in multiple sclerosis. This methodological approach will provide multiplex, spatially resolved molecular data that will not only define relationships between FGF expression and other molecular events within lesions, but will allow us to explore in unprecedented detail the identity of the effector pathways contributing to lesion formation.
- Techniques to be used: MALDI-IMS, immunopathology, bioinformatics, cell culture (for validation of specific pathways)
- References:1. Trapp BD, Nave KA (2008) Multiple sclerosis: an immune or neurodegenerative disorder? Annu Rev Neurosci. 31:247.
2. Lassmann H, van Horssen J, Mahad D. (2012) Progressive multiple sclerosis: pathology and pathogenesis. Nat Rev Neurol. 8(11):647.
3. Hagemeier K, Brück W, Kuhlmann T. (2012) Multiple sclerosis - remyelination failure as a cause of disease progression. Histol Histopathol. 27(3):277.
4. Schwamborn K & Caprioli R (2010) Molecular imaging by mass spectrometry — looking beyond classical histology. Nat Rev Cancer 10; 639.
- Contact: Professor Chris Linington (Christopher.firstname.lastname@example.org) Professor of Neuroimmunology, Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow
The immune system provides vital protection against infection, and can be manipulated by vaccination to provide life-long resistance to pathogens. However, immune and inflammatory responses also make a major contribution to a spectrum of human pathologies, from chronic inflammatory disease, allergy and autoimmunity, neuroinflammatory disorders and brain immune interactions, to heart disease and cancer.
Research in the Centre for Immunobiology within the Institute for Infection, Immunity and Inflammation is focused on generating a molecular and cellular understanding of the immune system in health and disease, and applying this knowledge to the development of novel therapeutics. This is built on close interactions between an excellent cohort of scientists and clinicians within the Centre, and on the networks of collaborators they have established with researchers in the rest of the Institute, elsewhere in the University, and further afield.
Our staff and students benefit from access to state-of-the-art laboratory facilities in the Sir Graeme Davis building at the heart of the University and in clinical units in hospitals across Glasgow. We have expertise in a broad range of techniques, including molecular biology, ‘Omics, cell biology, multiparameter flow cytometry, intravital imaging, and in vivo models of disease, and these approaches allow us to explore the immune system at the molecular, cellular and whole organism level.
PhD programmes in virology last 3-4 years and are based on individual research projects covering the interest of the supervisor.
The PhD programme in Immunobiology is based on individual research projects covering an exciting range of topics, with specific areas of interest including (in alphabetical order):
- Cancer and leukaemia.
- Chemokines and cell migration.
- Cytokine biology.
- Dendritic cell biology.
- Imaging the immune response.
- Infectious disease.
- Intestinal immunity.
- Intracellular signalling and transcriptional regulation.
- Lymphocyte biology.
- Neuroimmunology, including repair strategies forbrain repair following immunologically mediated injury (Multiple Sclerosis, Guillain-Barré syndrome) and spinal cord injury using glial/stem cell transplantation and antibody profiling.
- Tissue injury and repair; focus on regenerative medicine.
All our postgraduate research students are allocated a supervisor who acts as the main source of academic support and research mentoring.
You may want to identify a potential supervisor and contact them to discuss your research proposal before you apply.
Awarded or expected 1st class or high upper 2nd class BSc degree.
English Language requirements for applicants whose first language is not English.
Fees and funding
- £4,121 UK/EU
- £18,900 outside EU
Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.
Additional fees for all students:
- Submission by a research student £440
- Submission for a higher degree by published work £890
- Submission of thesis after deadline lapsed £140
- Submission by staff in receipt of staff scholarship £680
- Research students registered as non-supervised Thesis Pending students (50% refund will be granted if the student completes thesis within the first six months of the period) £250
- General Council fee £50
- Depending on the nature of the research project, some students will be expected to pay a bench fee to cover additional costs. The exact amount will be provided in the offer letter.
- £4,195 UK/EU*
- £19,500 outside EU
Prices are based on the annual fee for full-time study. Fees for part-time study are half the full-time fee.
* We expect that tuition fees for EU students entering in 2017 will continue to be set at the same level as that for UK students. However, future funding arrangements for EU students will be determined as part of the UK’s discussions on its future relationship. If you are thinking of applying for 2017 entry, we would encourage you to do so in the usual way. For further information, please see the Research Councils UK statement on international collaboration and Universities UK Brexit FAQs for universities and students.
Additional fees for all students:
- Fee for re-submission by a research student: £460
- Submission for a higher degree by published work: £1,050
- Submission of thesis after deadline lapsed: £250
- Submission by staff in receipt of staff scholarship: £730
- Research students registered as non-supervised Thesis Pending students (50% refund will be granted if the student completes thesis within the first six months of the period): £300
- Registration/exam only fee: £150
- General Council fee: £50
A 10% discount is available to University of Glasgow alumni. This includes graduates and those who have completed a Junior Year Abroad, Exchange programme or International Summer School at the University of Glasgow. The discount is applied at registration for students who are not in receipt of another discount or scholarship funded by the University. No additional application is required.
The College of Medical, Veterinary and Life Sciences Graduate School provides a vibrant, supportive and stimulating environment for all our postgraduate students. We aim to provide excellent support for our postgraduates through dedicated postgraduate convenors, highly trained supervisors and pastoral support for each student.
Our over-arching aim is to provide a research training environment that includes:
- provision of excellent facilities and cutting edge techniques
- training in essential research and generic skills
- excellence in supervision and mentoring
- interactive discussion groups and seminars
- an atmosphere that fosters critical cultural policy and research analysis
- synergy between research groups and areas
- extensive multidisciplinary and collaborative research
- extensive external collaborations both within and beyond the UK
- a robust generic skills programme including opportunities in social and commercial training
If you study with us, you will join a community of 26 postgraduate taught and 150 postgraduate research students. Our Institute of Infection, Immunity and Inflammation brings together world-leading basic, applied, clinical and translational researchers to study infection with a focus on the viral, parasitic and bacterial pathogens of both humans and animals, and immunology and inflammation with a focus on chronic inflammatory diseases.
Despite the continual development of new therapies, antibiotics and vaccines, chronic inflammatory and infectious diseases still pose persistent health threats. We aim to:
- understand the basic science of the immune systems and how the immune system can inturn affect disease outcome understand the biology of parasites, viruse and bacteria and the interactions with their hosts, that in turn leads to high levels of infectious diseases worldwide
- develop therapies (drugs and vaccines) targeted on these processes
- explore new treatments and strategies in clinical and translational medicine.
- MRC-University of Glasgow Centre for Virus Research
- Wellcome Centre for Molecular Parasitology
- ARUK Centre for Experimental Arthritis Research
We offer a wide range of cutting-edge research facilities, including:
- core facilities in fluorescence activated cell sorting analysis
- histology and state-of-the-art imaging
- IVIS imaging system
- high content screening microscopy
- mass spectrometry
- an X-ray capable FX Pro bioluminescence imaging system
- a protein purification service
- a wide range of molecular, immunological and biochemical analysis tools.
These excellent facilities underpin a bench to bedside approach that will equip you with training complementary to a range of career options, and you can tailor your study pathway to the precise aspects of infection and immunology that suit your objectives. Through their research interests in drug development, vaccines and diagnostics, many of our project supervisors have strong links with industry.How to apply