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Dr Anne Pesenacker
Institute of Immunity and Transplantation, Royal Free
Rowland Hill Street
London
N/A
NW3 2PF
Tel: 020 8016 8191
Appointment
  • Research Fellow
  • Div of Infection & Immunity
  • Faculty of Medical Sciences
Biography

Dr. Anne M Pesenacker’s research focuses on how regulatory T cell (Treg) function is controlled in health versus autoimmunity. In 2013, Anne completed her PhD with Dr. Lucy Wedderburn at UCL as part of the Oliver Bird PhD programme, where she defined and characterised CD161+ Tregs as the subset that is poised to produce pro-inflammatory cytokines in health and enriched in the inflamed joint of Juvenile Idiopathic Arthritis.  
Dr. Pesenacker continued her training in the Levings lab at UBC’s BC Children’s Hospital Research Institute in Vancouver, CA, where she held postdoctoral fellowships from the Juvenile Diabetes Research Foundation to focus on molecular mechanisms of Treg function in autoimmune diabetes. In particular, she developed a Treg gene signature that can be used as a biomarker for Treg fitness and predict disease activity. Dr. Pesenacker also discovered that mouse and human Tregs produce chemokines upon activation. She established methods to knock out receptors in primary human Tregs via CRISPR-Cas and applied the technology to elucidate the role of the TNF receptors in Treg function and survival.  Moreover, Dr. Pesenacker initiated a new laboratory-based research program in collaboration with the Rheumatology unit at BC Children’s Hospital.
In 2018, Dr. Pesenacker moved to UCL’s Institute of Immunity and Transplantation to start her own research group with a Versus Arthritis career development fellowship. Her work focuses on the role of co-stimulatory and co-inhibitory receptors in primary human Treg function in health and disease.

Research Themes
Research Summary
CD4+ Regulatory T cells (Tregs) are crucial to maintain tolerance, balancing effector T cell responses to harmful agents and suppressing unwanted responses. However, too little control may lead to autoimmunity (e.g. juvenile idiopathic arthritis or type 1 diabetes), while too much control may contribute to the development of cancers. Co-stimulatory and co-inhibitory receptors are crucial to determine functional outcomes upon activation. We found an imbalance of co-receptor expression at the site of inflammation and mutations in co-receptor genes have been associated with autoimmunity. We focus on the co-receptor family CD226, TIGIT and CD96; receptors highly expressed on Tregs but with little understanding of their function. We use cellular and molecular immunology techniques, including the cutting-edge gene-editing system CRISPR-Cas9, to elucidate the CD226, TIGIT and CD96 signalling, receptor-receptor and receptor-ligand interactions and study their role in primary human Treg function in health and disease.
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