Postgraduate research 

Infection, Immunity & Inflammation PhD/iPhD/MD/MSc (Research)

Start dates for incoming postgraduate research students

1 October 2020 is the preferred date to start your PhD [or the date on your offer letter].

We will run a full on-line induction and training programme that may be taken remotely for the first month. Most of our doctoral researcher training programme will also be available online and we will offer many remote opportunities to help you become part of the Graduate School and wider University community.  

Research that involves laboratory work may start following the completion of induction (all labs are currently up and running).

Some types of research (such as non-laboratory work) and supervision can be carried out entirely remotely and this may be the most appropriate way for you to work at the moment.  Contact your supervisor, if you believe this applies to your research to discuss requirements for home/remote working. You may also require the agreement of the subject, school or institute convener if you wish to carry out your PhD remotely for a fixed period. You may not continue remotely unless an adequate plan is agreed to ensure sufficient work can be undertaken prior to starting the experimental work. It is important that starting remotely does not affect the overall PhD timescale.

Delayed start dates

We understand there may be good reasons to delay:

  • If it is necessary to travel to Glasgow to begin your research, but there are restrictions preventing travel at this time, then a delay to 5 January 2021 is encouraged [when we will run full on-line induction and training programme]. You may also delay to another start time with the agreement of your supervisor and Graduate School.
  • For subjects where laboratory work is required to commence immediately following on-line induction and training and you are unable to come to Glasgow, you should consider delaying your start-date. Contact your supervisor or the Graduate School in this instance.
  • If your research involves objects, artefacts, archives or fieldwork, you should discuss this with your supervisor. Some kinds of work may be able to be started remotely; in other cases, it may be advisable to delay the start-date.
  • External government sponsors may prefer a delay and the University is happy to support this.

From our point of view, there is no disadvantage in deferring your PhD to a later agreed start date. Scholarship holders should check that this can still be provided with a delayed start.

Office and study space

At present, current staff and research students are not using office spaces on campus. We do not have a confirmed date for the return to office use, but all work that can be undertaken off-campus (ie is not lab-based) should be done at home or remotely at present.

Some study spaces are becoming available on campus with a booking system in place, such as the postgraduate study space in the University Library.

International/EU students remotely starting a funded PhD

You should check with your funder that you can be paid a stipend if you are not in the UK. If you are in receipt of a scholarship, you should contact the Graduate School for advice on opening a bank account to allow stipend payments.


Immunology research includes cytokine and chemokine biology, immune cell signalling, advanced imaging technologies, and cellular & gut immunology. Our translational efforts are focused on rheumatoid arthritis, dermatology, respiratory & central nervous system immune & inflammatory diseases.

Research projects

Self-funded PhD opportunities


Investigating the molecular mechanisms underlying the cellular decision to initiate inflammation

Supervisor: Ruaidhrí Carmody

  • Project outline: The ability of the innate immune system to discriminate between stimuli that pose little danger and those that threaten the host is a key determinant of human health. The concentration of microbial-associated molecules that activates an innate inflammatory response is determined by the activation threshold of key signalling pathways. This is an important mechanism used by innate immune cells to distinguish between threats that should be tolerated and those that require a strong inflammatory response. This project is based on our recent findings that the stability of TPL-2 (MAP3K8), a key activator of the mitogen activated protein kinase (MAPK) pathway, controls the cellular decision to respond to inflammatory stimuli. Our studies so far have identified the nucleus as the key site regulating the stability of TPL-2. This project will investigate the regulation MAPKs in the nucleus during innate immune cell responses; explore novel functions of MAPKs in the nucleus; and investigate the impact of altering MAPK activation on cellular responses to inflammatory stimuli. The findings will provide fundamental insights into the regulation of the cellular response to inflammatory stimuli and contribute to the development of novel strategies for the therapeutic control of inflammation.
  • Summary aim: This project will investigate regulation and function of MAPKs in the nucleus during innate immune cell activation.

  • Techniques to be used:CRISPR/Cas9 gene editing, molecular biology (including site directed mutagenesis), chromatin immunoprecipitation, immunoblotting, cell culture, real-time PCR.

  •, 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
  • Also see



The NF-ĸB transcription factor

Supervisor: Ruaidhrí Carmody

  • Project outline: The NF-ĸB transcription factor is a master regulator of the immune response and plays a critical role in inflammatory disease by mediating the expression of pro-inflammatory factors. The NF-ĸB-directed transcription of genes that promote cell survival and proliferation also implicates it as an important factor in cancers and neurodegenerative disorders. The key roles for NF-ĸB in the pathogenesis of these and other diseases have established it as an important therapeutic target, which to date remains unharnessed. Previous strategies focussed on inhibiting the IKK kinases, critical activators of NF-ĸB, have failed to make clinical impact due to severe side-effects, and so new approaches to targeting NF-ĸB for therapeutic benefit are required. This project aims to exploit the regulation of NF-ĸB by the ubiquitin proteasome system in order to inhibit NF-ĸB mediated inflammatory responses. The ubiquitin-triggered proteasomal degradation of NF-ĸB is a major limiting factor in the expression of pro-inflammatory genes. We have previously identified the deubiquitinase USP7 as a key regulator of NF-ĸB transcriptional activity by reversing NF-ĸB ubiquitination and preventing its proteasomal degradation. We have extended these initial findings to identify a distinct NF-ĸB binding site in USP7 that selectively mediates the interaction of USP7 with NF-ĸB. We hypothesise that this binding site could be targeted to selectively inhibit NF-ĸB-directed inflammatory responses by promoting its ubiquitination and degradation. This project is a structure-function based study of the USP7 and NF-ĸB interface that will define the NF-ĸB binding site and the functional impact of its disruption. The results will facilitate the rational structure-led design of substrate-selective inhibitors of USP7 to inhibit NF-kB mediated inflammatory responses.
  • Summary aim: This project will investigate the potential to inhibit inflammation by inhibiting the deubiquitination of NF-κB by USP7.

  • Techniques to be used: CRISPR/Cas9 gene editing, molecular biology (including site directed mutagenesis), protein purification and X- ray crystallography, proteomics and transcriptomics.

  •, 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
  • Also see



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 ( 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



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:



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 (, Level 3, Glasgow Biomedical Research Centre, Institute of Infection, Immunity and Inflammation,College of MVLS University of Glasgow, 120, University Place, Glasgow G12 8TA



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 ( 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:



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:



Investigating Immune Pathways in Cardiovascular Diseases

Supervisor: Dr Pasquale Maffia

  • Project outline: Immune responses play key roles in cardiovascular diseases (CVD) such as atherosclerosis and hypertension. By using a broad range of vascular, immunological and omics techniques we aim to study the net contribution of specific immune pathways to CVD in humans and experimental models.
  • Techniques to be used: The project will provide training in both vascular biology and immunology, including flow cytometry, microscopy and single-cell omics.
  • References:

    1. MacRitchie N, Grassia G, Noonan J, Cole JE, Hughes CE, Schroeder J, Benson RA, Cochain C, Zernecke A, Guzik TJ, Garside P, Monaco C, Maffia P. The aorta can act as a site of naive CD4+ T cell priming. Cardiovasc Res. 2019 Apr 13. pii: cvz102. doi: 10.1093/cvr/cvz102. [Epub ahead of print].

    2. Noonan J, Asiala SM, Grassia G, MacRitchie N, Gracie K, Carson J, Moores M, Girolami M, Bradshaw AC, Guzik TJ, Meehan GR, Scales HE, Brewer JM, McInnes IB, SaJar N, Faulds K, Garside P, Graham D, Maffia P. In vivo multiplex molecular imaging of vascular inflammation using surface-enhanced Raman spectroscopy. Theranostics. 2018;8:6195-6209.

    3. Welsh P, Grassia G, Botha S, SaJar N, Maffia P. Targeting inflammation to reduce cardiovascular disease risk: a realistic clinical prospect? Br J Pharmacol. 2017;174:3898-3913.

    4. Hu D, Mohanta SK, Yin C, Peng L, Ma Z, Srikakulapu P, Grassia G, MacRitchie N, Dever G, Gordon P, Burton FL, Ialenti A, Sabir SR, McInnes IB, Brewer JM, Garside P, Weber C, Lehmann T, Teupser D, Habenicht L, Beer M, Grabner R, Maffia P, Weih F, Habenicht AJ. Artery Tertiary Lymphoid Organs Control Aorta Immunity and Protect against Atherosclerosis via Vascular Smooth Muscle Cell Lymphotoxin Beta Receptors. Immunity. 2015;42:1100-15.

  • Contact: Pasquale Maffia (, 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



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 (, 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



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 ( 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 & 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.

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):

  • atherosclerosis
  • bioinformatics
  • 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
  • osteoimmunology
  • rheumatology
  • tissue injury and repair; focus on regenerative medicine

Study options


  • Duration: 3/4 years full-time; 5 years part-time

Individual research projects are tailored around the expertise of principal investigators.

MSc (Research)

  • Duration: 1 year full-time; 2 years part-time

MD (Doctor of Medicine)

  • Duration: 2 years full-time; 4 years part-time (for medically-qualified graduates only)

Integrated PhD programmes (5 years)

Our integrated PhD allows you to combine Masters level teaching with your chosen research direction in a 1+3+1 format. 

International students with MSc and PhD scholarships/funding do not have to apply for 2 Visas or exit and re-enter the country between programmes. International and UK/EU students may apply.

Year 1

Taught masters level modules are taken alongside students on our masters programmes. Our research-led teaching supports you to fine tune your research ideas and discuss these with potential PhD supervisors. You will gain a valuable introduction to academic topics, research methods, laboratory skills and the critical evaluation of research data. Your grades must meet our requirements in order to gain entry on to a PhD research programme. If not, you will receive the Masters degree only.

Years 2, 3 and 4

PhD programme with research/lab work, completing an examinable piece of independent research in year 4.

Year 5

Thesis write up.

All applicants must have full funding before starting their iPhD programme.

Entry requirements

PhD programmes

Awarded or expected First-class or high Upper Second-class BSc degree.

Integrated PhD programmes

Upper 2nd class honours degree or international equivalent in a relevant subject area.

English Language requirements for applicants whose first language is not English.

Fees and funding



  • UK fee to be confirmed by (2020/21 fee was £4,407)
  • International & EU: £23,000

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:

  • Re-submission by a research student £540
  • Submission for a higher degree by published work £1,355
  • Submission of thesis after deadline lapsed £350
  • Submission by staff in receipt of staff scholarship £790

Depending on the nature of the research project, some students will be expected to pay a bench fee (also known as research support costs) to cover additional costs. The exact amount will be provided in the offer letter.

Alumni discount

We offer a 10% discount to our alumni on all Postgraduate Research and full Postgraduate Taught Masters programmes. This includes University of Glasgow graduates and those who have completed Junior Year Abroad, Exchange programme or International Summer School with us. 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.


2020/21 fees

  • £4,407 UK/EU
  • £21,920 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:

  • Re-submission by a research student £525
  • Submission for a higher degree by published work £1,315
  • Submission of thesis after deadline lapsed £340
  • Submission by staff in receipt of staff scholarship £765

Depending on the nature of the research project, some students will be expected to pay a bench fee (also known as research support costs) to cover additional costs. The exact amount will be provided in the offer letter.

Alumni discount

We offer a 20% discount to our alumni commencing study in Academic session 2020/21, on all Postgraduate Research and full Postgraduate Taught Masters programmes. This includes University of Glasgow graduates and those who have completed a Study Abroad programme or the Erasmus Programme at the University of Glasgow. This discount can be awarded alongside other University scholarships. 

Funding for EU students

The Scottish Government has confirmed that fees for EU students commencing their studies 2020/21 will be at the same level as those for UK student.




The College of Medical, Veterinary & 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 overarching 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

Research environment

If you study with us, you will join a community of 26 postgraduate taught and 150 postgraduate research students. Our Institute of Infection, Immunity & 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

Research centres

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

Identify potential supervisors

All Postgraduate Research Students are allocated a supervisor who will act 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. Please note, even if you have spoken to an academic staff member about your proposal you still need to submit an online application form.

You can find relevant academic staff members with our staff research interests search.

Gather your documents

Before applying please make sure you gather the following supporting documentation:

  1. Final or current degree transcripts including grades (and an official translation, if needed) – scanned copy in colour of the original document.
  2. Degree certificates (and an official translation, if needed): scanned copy in colour of the original document.
  3. Two references on headed paper and signed by the referee. One must be academic, the other can be academic or professional. References may be uploaded as part of the application form or you may enter your referees contact details on the application form. We will then email your referee and notify you when we receive the reference.  We can also accept confidential references direct to, from the referee’s university or business email account.
  4. Research proposal, CV, samples of written work as per requirements for each subject area.

Apply now

I've applied. What next?

If you have any other trouble accessing Applicant Self-Service, please see Application Troubleshooting/FAQs. 

Contact us

Before you apply

PhD/MSc/MD: email

iPhD: email

After you have submitted your application

PhD/MSc/MD/iPhD: contact our Admissions team

Any references may be submitted by email to: