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Research

Immune regeneration and modulation

Haematopoietic stem cell transplantation (commonly known as bone marrow transplantation) is the oldest stem cell therapy, having been introduced into clinical practice in the 1960’s. In many cases where it is used, the curative effect of the transplant relies on the development of an effective immune system in the patient after the transplant. My research is concerned with how that immune system develops – what environmental and genetic factors influence the immune development and how we can shape the immune system to optimise the benefit to the patient.

Paul Travers

Affiliated researcher
Reader in clinical sciences / Course director MSc in regenerative medicine, CRM, University of Edinburgh
0131 651 9500
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Aims and areas of interest

My primary aim is in understanding the development of the human immune repertoire and how this is altered in disease and after therapy such as haematopoietic stem cell transplantation (HSCT).

Optimising the immune repertoire

  1. Stem cell transplantation We have been investigating immune system parameters in patients undergoing HSCT that are associated with outcome, and have identified a significant association between relapse mortality, regulatory T cells and patterns of cytokine expression. This may provide a basis for stratifying patients prior to transplant and provide a route for intervention to improve the outcome for those patients currently at high risk of post-transplant mortality.
  2. Stress and the immune repertoire We have identified a significant deficit In thymic function in elite athletes, most likely as a consequence of stress induced by their intense training regimes. We are interested in further clarifying this effect, how long it might persist and whether it might create a long term immune deficit. Moreover, we are interested in asking what level of stress is required to induce this deficit and whether other sectors of the population may be at risk. 
  3. Genetic polymorphism and autoimmunity PTPN22 is a regulatory tyrosine phosphatase expressed in lymphoid cells which functions to control signalling through the antigen receptor of these cells. A common polymorphism in PTPN22 is strongly associated with a number of autoimmune diseases and we are investigating the impact of this polymorphism on the immune repertoire and how this may bias the immune system towards autoimmunity.
Funders
  • University of Edinburgh
Collaborators
  • Prof Mike Gleeson (Loughborough)
  • Dr Adria Prieto-Hinojosa (Mexico)
  • Drs Alexandra Senegaglia and Dr Noemi Farah Pereira (Brazil)
  • Prof Rose Zamoyska (Edinburgh)