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Full NameProfessor Denise Fitzgerald

Department:Wellcome-Wolfson Institute for Experimental Medicine

Organisation:Queen's University Belfast

Email Address:Email hidden; Javascript is required.

Research Fields
  • infectious disease and the immune system
  • cell and developmental biology/regenerative medicine
  • neuroscience and mental health
Postgrad Medical Specialties
  • Psychiatry
  • Ophthalmology
  • Paediatrics
  • Pathology
  • Public Health
Medical Subspecialties
  • Adolescent medicine
  • Dementia
  • Immunology
  • Neurology
  • Neurophysiology
  • Neuropsychiatry
  • Physiology
  • Psychiatry
My Work

The Fitzgerald lab is a Regenerative NeuroImmunology research group at QUB with a particular focus on Multiple Sclerosis (MS), an immune-mediated, demyelinating disorder of the Central Nervous System (CNS). The central goal of our research is to identify new strategies to treat MS and other inflammatory and demyelinating conditions.

We are particularly interested in the process of myelin repair (remyelination) and aim to identify novel therapeutic targets to promote remyelination in MS. To address this goal, we are uncovering new cellular and molecular cues from the immune system that influence the response to neurological damage and promote successful progenitor cell maturation to repair damaged tissue. We also conduct a research programme on the pathogenesis of autoimmune inflammation with an emphasis on T cell biology.

Our hard-working team consists of scientists from the fields of Neuroscience, Regenerative Biology and Immunology who work together to study neuro-immune cellular communication and interaction, supported by international collaborators including in Ophthalmology. Through our research we are gaining new insights into the influence of the immune system and inflammation on demyelination and remyelination in the CNS.

Regulatory T cells promote myelin regeneration in the central nervous system. Dombrowski Y, et al., Nature Neuroscience. 2017 May;20(5):674-680. doi: 10.1038/nn.4528.

Potential Projects

There are a range of potential projects that can be facilitated in our lab including topics on regenerative immune profiling in clinical cohorts (blood and CNS), fundamental neural stem and progenitor cell biology, fundamental immunology, experimental modelling of demyelination and remyelination, retinal imaging in clinical cohorts, mechanistic studies in clinical trial cohorts and neuropathological studies with a unique human brain bank. Specific interests can be discussed with the PI and tailored projects appropriate to the resources and collaborators available (San Francisco, Philadelphia, Cambridge, Edinburgh, Dublin) can be developed.

The following is an overall summary of our main programme of research to 2021:

Myelin, the supportive insulation that wraps around nerve axons in the Central Nervous System (CNS) is produced by oligodendrocytes. When myelin is damaged in conditions like Multiple Sclerosis (MS), a repair response can be activated. This should result in the maturation of oligodendrocyte progenitor cells into myelin-regenerating oligodendrocytes that re-ensheath axons (remyelination) and restore neurological function. However when remyelination fails, as is common in Multiple Sclerosis, patients can develop permanent disability. Recently, immune cells have been implicated in regulation of this regenerative process however little is known about the role of T cells in remyelination, despite decades of research into T cell-mediated myelin damage (demyelination). We have discovered that the regulatory subset of T cells (Treg)accelerate myelin regeneration in the brain and spinal cord. Treg instruct oligodendrocyte progenitor cells to differentiate into myelin-producing oligodendrocytes, in part via Treg-secreted CCN3, a novel matricellular protein in remyelination. By combining neuroscience, immunology and regenerative biology, this programme of work will determine how different types of T cells influence remyelination and examine whether the progression of demyelinating diseases like MS alters these fundamental functions of T cells in CNS regeneration.