Dr David Bending

Institute of Immunology and Immunotherapy
Birmingham Fellow

Contact details

Telephone: +44 (0)121 414 3634
Email: d.a.bending@bham.ac.uk
Twitter: @BendingLab

Address: Institute of Immunology and Immunotherapy
College of Medical and Dental Sciences
Room 436 Institute of Biomedical Research
University of Birmingham
B15 2TT

David Bending is a group leader within the Institute of Immunology and Immunotherapy. The lab’s research is focused on understanding the cellular and molecular mechanisms that control T-cell differentiation, function and regulation.

Qualifications

PhD in Immunology 2012
MA hons 2011
BA hons 2007

Biography

David completed his PhD in Immunology in the laboratory of Anne Cooke, at the University of Cambridge in 2011, where he was amongst the first to reveal the plasticity of T-helper 17 (Th17) cells during autoimmune disease. In 2011, he obtained an Arthritis Research UK Fellowship to study the stability of Foxp3 expression in Treg cells in childhood Arthritis, at UCL. In 2015, he joined Masahiro Ono's group at Imperial College London, where together they developed a novel approach to reveal T-cell receptor signalling dynamics and real-time Foxp3 expression using the Timer of cell kinetics and activity (Tocky) system. In 2018 he moved to Birmingham to start his own research group focusing on how T-cell receptor signalling dynamics are related to T-cell effector and regulatory functions during immune responses.

Postgraduate supervision

Bending lab is open to applications from potential PhD students, with an enthusiastic interest in T-cell immunology. Please email d.a.bending@bham.ac.uk

Research

Current research projects:

1) How do T-cell receptor signalling dynamics control IL-10-producing T-cell differentiation

This project employs the state of the art Tocky system to understand how different patterns of T-cell receptor (TCR) signalling regulate the differentiation and function of IL-10 producing T-cells. In particular, the group is interested in revealing how peptide immunotherapy modulates TCR signalling to ameliorate disease in multiple sclerosis.

2) Understanding the role of T-cell receptor signalling dynamics in driving Th17 and Th1 responses, and regulating T-cell plasticity

Th17 and Th1 responses are elicited in response to different types of immune challenge. The group seeks to understand the role of TCR signalling in re-directing Th17 cells into the Th1 lineage.

3) Revealing the mechanism of action of T-cell targeting immunotherapies

The group have identified several membrane receptor targets that identify functionally important T-cell subsets. The group seeks to understand how targeting these membrane proteins through immunotherapies, such as anti-OX40 antibody, modulates the immune response.

Publications

Bending, D., Paduraru, A., Ducker, C., Prieto-Martin, P., Crompton, T. & Ono, M. A temporally dynamic Foxp3 autoregulatory transcriptional circuit controls the effector Treg programme. EMBOJ, in press (2018).

Bending, D., Prieto Martin, P., Paduraru, A., Ducker, C., Marzaganov, E., Laviron, M., Kitano, S., Miyachi, H., Crompton, T. & Ono, M. A Timer for analyzing temporally dynamic changes in transcription during differentiation in vivo. J Cell Biol, doi:10.1083/jcb.201711048 (2018).

Bending, D. & Ono, M. Interplay between the skin barrier and immune cells in patients with atopic dermatitis unraveled by means of mathematical modeling. J Allergy Clin Immunol 139, 1790-1792, doi:10.1016/j.jaci.2017.03.015 (2017).

Bending, D. & Ono, M. FoxP3 partners up. Nat Immunol 18, 1181-1183, doi:10.1038/ni.3852 (2017).

Bending, D., Giannakopoulou, E., Lom, H. & Wedderburn, L. R. Synovial Regulatory T Cells Occupy a Discrete TCR Niche in Human Arthritis and Require Local Signals To Stabilize FOXP3 Protein Expression. J Immunol 195, 5616-5624, doi:10.4049/jimmunol.1500391 (2015).

Piper, C., Pesenacker, A. M., Bending, D., Thirugnanabalan, B., Varsani, H., Wedderburn, L. R. & Nistala, K. T cell expression of granulocyte-macrophage colony-stimulating factor in juvenile arthritis is contingent upon Th17 plasticity. Arthritis Rheumatol 66, 1955-1960, doi:10.1002/art.38647 (2014).

Bending, D., Pesenacker, A. M., Ursu, S., Wu, Q., Lom, H., Thirugnanabalan, B. & Wedderburn, L. R. Hypomethylation at the regulatory T cell-specific demethylated region in CD25hi T cells is decoupled from FOXP3 expression at the inflamed site in childhood arthritis. J Immunol 193, 2699-2708, doi:10.4049/jimmunol.1400599 (2014).

Pesenacker, A. M., Bending, D., Ursu, S., Wu, Q., Nistala, K. & Wedderburn, L. R. CD161 defines the subset of FoxP3+ T cells capable of producing proinflammatory cytokines. Blood 121, 2647-2658, doi:10.1182/blood-2012-08-443473 (2013).

Morrison, P. J., Bending, D., Fouser, L. A., Wright, J. F., Stockinger, B., Cooke, A. & Kullberg, M. C. Th17-cell plasticity in Helicobacter hepaticus-induced intestinal inflammation. Mucosal Immunol 6, 1143-1156, doi:10.1038/mi.2013.11 (2013).

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