PhD projects available through TRAM
The interaction between naïve T lymphocytes (T cells) and Dendritic Cells (DC), called the immune synapse, underpins the decision by the immune system to switch ‘on’ or ‘off’. In autoimmune diseases such as rheumatoid arthritis, the immune system makes the wrong decision to switch on, when it should be switching off. Compounds that can re-educate the immune system to make the right decision therefore have potential to treat disease. We have pioneered the use of advanced microscopy techniques to analyse the immune synapse. This has allowed us to screen thousands of chemicals, to identify synapse disruptors, that can perform immune re-education and may therefore have potential in treatment of autoimmune disease. We are currently working with Prof Carl Goodyear to characterise and understand the effects of synapse disruptors in treatment-resistant rheumatoid arthritis.
- Identify targets of lead aptamers. We will use pull down assays to selectively isolate aptamer binding partners from target cell homogenates, followed by identification using mass spectrometry.
- Understand the mechanism of action of lead aptamers. This will involve RNA sequencing of treated dendritic cells to identify pathways modulated by aptamer exposure.
- Assess in vivo activity. Mouse models of arthritis will be used to determine whether the aptamers can resolve inflammation.
- Evaluate functionality in arthritis. Using T cells and DCs isolated from the peripheral blood of patients with arthritis, we will analyse how the aptamers influence their interactions compared with existing drug treatments.
- Could there be a role for B cell depletion in the management of large vessel vasculitis?
- Pioneering Full Body PET to dynamically map the immune system in patients with inflammatory arthritis
Professor of Gastroenterology | The Gut Translational Research Group
Gwo-Tzer.Ho@glasgow.ac.uk
- Defining the homeostatic circuits that underpin the tissue states that determine inflammation in gut and joints
- Characterising the evolution of inflammation in joints and inflammation following immune-therapy in IBD
- Why IMIDs fail to resolve: age dependent breakdown of tissue homeostasis in inflammatory arthritis
- Ageing-associated determinants of response and resistance in inflammatory arthritis
I lead the TARGET LUPUS programme, which brings together international experts to develop better ways of treating childhood onset lupus. This includes the world’s largest study of young people with lupus, cSLE T2T Global, helping us understand outcomes and care across different countries. I also lead the NEPHROTARGET study, which looks at whether urine biomarkers can help guide treatment decisions.
I’m the paediatric lead for the national NIHR FIRST trial, which is testing whether using Rituximab earlier can improve outcomes in both children and adults with lupus. Alongside my lupus research, I also lead a functional MRI study running at four sites across the UK exploring how the brain processes pain in young people with arthritis.
- Predicting poor outcomes in Rheumatic Diseases affecting children and adults using real world data
- Development and testing of a digital tool to support treat to target (T2T) in Childhood Lupus
- Understanding obesity across the life-course in Paediatric Rheumatic Diseases: prevalence, inequalities and clinical impact
- Neuroimmune signatures of pain in paediatric rheumatic diseases
- Immunology-focused PhD: “Unravelling effect of brain-driven pain on peripheral immune set point in psoriatic arthritis: an epigenetic and transcriptomic approach”
- Neuroscience-focused PhD: “Targeting the brain to treat pain: mechanistic insights into transcranial magnetic stimulation in inflammatory arthritis”
Professor of Inflammation Medicine and Rheumatology
Stefan.siebert@glasgow.ac.uk
Potential PhD projects include laboratory-based studies using samples and data from these and other studies to investigate key immune/ metabolic disease pathways and to identify clinically relevant biomarkers in PsA, RA and obesity. There are also more data driven projects using data from existing studies or data-linkage in the trusted research environment (TRE) to investigate key aspects and outcomes of these conditions.
- How do we reprogramme the immune system to re-establish health in chronic inflammatory diseases
- Defining theragnostic biomarkers in rheumatic diseases to inform therapeutic decisions in clinical practice
Professor of Immune Pathology and Homeostasis
Mariola.Kurowska-Stolarska@glasgow.ac.uk
To maximise the impact of tissue discoveries, our lab follows a bedside-to-bench-and-back scientific approach, in which human and mouse research strategies are fully integrated to advance understanding of basic tissue biology and drive clinical innovation. You will be embedded in an ex vivo and in vivo experimental tissue biology lab that is closely linked with the experimental medicine tissue lab at Gemelli Hospital in Rome, led by Professor Stefano Alivernini. This partnership enables a fully integrated basic science and translational research approach within a single project.
- Identifying the cellular and molecular mechanisms that drive the localization of inflammation in joints of individuals at risk of Rheumatoid Arthritis.
- Investigating the role of synovial tissue AXL⁺ DC2 cells in maintaining local tissue and systemic immune tolerance.
- Studying the role of SPP1⁺ synovial tissue macrophages in driving disease flares in Rheumatoid Arthritis patients in remission.
My research centres on the study of multiple arthritic diseases, unified by an overarching focus on the cellular and molecular processes that operate within the joint.
My work in osteoarthritis concentrates on how bone contributes to the initiation and progression of joint degeneration. This research led to the investigation of energy metabolism within the joint, which has revealed pathways that may b e relevant across multiple arthritic conditions.
These mechanistic insights have steered a growing interest in psoriatic arthritis, particularly because clinical and mechanistic observations indicate that psoriatic arthritis can present with degenerative‑appearing changes and joint involvement patterns that resemble osteoarthritis.
To investigate these mechanisms, I use pre‑clinical mouse models that enable controlled replication of distinct inflammatory, degenerative, and structural features of joint disease. These systems allow detailed analysis of cellular interactions within the joint and facilitate the dissection of both common and divergent drivers of pathology in osteoarthritis and psoriatic arthritis.
In addition, I study how biological sex influences susceptibility and progression in osteoarthritis, and I investigate the molecular and cellular mechanisms underlying pain, focusing on the peripheral nervous system. Both sex‑specific differences and pain biology represent critical but underexplored contributors to disease heterogeneity and clinical burden across arthritic conditions.- Exploring the impact of Mechanical Stimulation in Psoriatic Arthritis
- Energy metabolism in the arthritic joint
My research focuses on understanding the immune mechanisms that sustain chronic granulomatous inflammation in giant cell arteritis (GCA), a severe form of vasculitis that can lead to irreversible tissue damage and relapse despite treatment. Funded by a Versus Arthritis Career Development Fellowship, my programme investigates how interactions between B cells, macrophages and multinucleated giant cells shape tissue pathology, influence therapeutic response, and determine disease persistence.
Using spatial and single-cell transcriptomics, BCR repertoire analysis, functional mono- and co-culture systems, and ex vivo artery explant models, we aim to define the immune circuits that drive inflammation within affected tissue. While centred on GCA, this work also explores whether similar mechanisms operate in other immune-mediated inflammatory diseases such as rheumatoid arthritis, Crohn’s disease and granulomatosis with polyangiitis, particularly in treatment-refractory or relapsing forms characterised by granulomatous inflammation.
My long-term goal is to use tissue-level immune profiling to move beyond disease labels and guide more precise, mechanism-driven treatment strategies aligned with the biology of active inflammation.
- Immune Memory in Giant Cell Arteritis and the Role of Memory B Cells in Disease Pathology and Relapse
- Targeting Multinucleated Giant Cells as a Strategy to Treat Chronic Granulomatous Inflammation
- Breaking the Inflammatory Circuit: B Cell-Macrophage Interactions in Giant Cell Arteritis
- Defining Conserved Tissue Immune Networks Across Granulomatous Immune-Mediated Inflammatory Diseases
The team in my lab focusses on cellular immunology, using a range of functional and computational tools to understand the mechanisms driving inflammatory disease. We primarily use samples from people with inflammatory bowel disease (IBD) and alopecia aerate (AA). We study cellular and mechanisms by which macrophages and dendritic cells control T cell responses in the skin and intestine, using our knowledge of the immune system to identify potentially-targetable mechanisms. We work closely with clinicians and basic scientists UK-wide to understand how to treat inflammatory disease, focussing on finding ways to restore tissue homeostasis after currently-available treatments have surpassed inflammatory pathways.
- Understanding common mechanisms to restore homeostasis in IMIDs
- Epithelial damage and repair in immune-mediated inflammatory disease
I am a professor of Respiratory Medicine at the University of Glasgow and my lab studies how inflammation causes lung damage and how we might intervene to stop this. We are now using observations made in rare lung diseases (e.g., Cystic Fibrosis) to inform further research into common lung diseases (e.g., COPD). We are very interested in how common inflammatory processes may cause inflammation across multiple organ systems. This is perhaps most interesting in people with RA who often have undiagnosed airways disease and have a common risk factor with COPD of smoking.
- Investigating airways disease in COPD
- Using clinical, radiological, and pathological data to characterise interstitial lung disease in RA and compare this to non-RA interstitial lung disease
If you would like to discuss these further, please contact tram@glasgow.ac.uk