Dr Sarah Dimeloe PhD

Dr Sarah Dimeloe

Institute of Immunology and Immunotherapy
Birmingham Fellow

Contact details

Address
Institute of Immunology and Immunotherapy
College of Medical and Dental Sciences
IBR, University of Birmingham
Edgbaston
Birmingham
B15 2TT

Sarah Dimeloe is a Birmingham Fellow working across the Institutes of Immunology and Immunotherapy (III), and Metabolism and Systems Research (IMSR).

Research in Sarah’s lab is focused on the metabolism of immune cells and how this underpins their role in health and disease.

Qualifications

  • PhD Immunology (2012)
  • MSc Immunology (2008)
  • MPharm Pharmacy (2004)

Biography

Sarah Dimeloe qualified with an MPharm (Hons) from the University of Nottingham in 2004.  She then completed her professional training as a pharmacist at Guy’s and St. Thomas’ NHS Foundation Trust. 

In 2007, Sarah undertook an MSc in Immunology at King’s College London (KCL), prior to completing her PhD in Immunology at KCL under the supervision of Professor Catherine Hawrylowicz.  During her PhD, Sarah investigated the biology of CD4+ T lymphocytes in allergic and asthmatic disease.

In 2012 Sarah moved to the University of Basel in Switzerland to undertake post-doctoral research in the laboratory of Professor Christoph Hess.  Here, Sarah began to investigate metabolic activity in T cells and how that relates to their important roles in health and disease. 

In 2017 Sarah was awarded a Birmingham Fellowship to establish her own research group at the University of Birmingham.

Postgraduate supervision

For any doctoral research enquiries, please email: s.k.dimeloe@bham.ac.uk

Research

Current research interests in Sarah Dimeloe’s lab focus on the metabolism and interlinked immune function of T lymphocytes in health and disease.

T lymphocytes comprise two subsets: CD4+ T cells, which co-ordinate immune responses against infections or cancers and CD8+ T cells, which can kill infected or cancerous cells of the body, as well as producing important cytokines (messenger molecules).  Following an immune response, “memory” populations of both of these cell types remain in the body, surveying for reappearance of a threat, to which they are able to rapidly respond, in order to protect us.

During her post-doctoral research in Basel, Sarah identified a key signal instructing the required changes in metabolism in order for CD4+ T cells to coordinate an immune response.  This signal was the binding of the innate immune molecule, complement C3b, to its receptor CD46 on the surface of CD4+ T cells.  Sarah additionally worked to define the key metabolic traits of memory T cells that enable them to perform their specialised role.  For example, Sarah identified that memory CD4+ T cells have large and complex mitochondria, enabling them to survive in, and patrol oxygen-poor environments like peripheral tissues of the body. She also contributed to work identifying that memory CD8+ T cells are metabolically “primed” to rapidly respond to threats.

In Birmingham, Sarah is now developing this research further to ask questions about how these “normal” metabolic functions are dysregulated in disease, and importantly, if such perturbations can be targeted to restore optimal T cell function and protection from disease.  Specifically, Sarah is investigating changes in the use of key nutrients by T cells during their development and in disease states.  Additionally, she working to identify components of diseased tissues that may subvert T cell metabolism and interlinked immune function and delineate the mechanisms involved, with the aim of discovering potential therapeutic targets. One experimental approach that Sarah is using to ask these questions is to perform high-resolution metabolic tracing analyses, by working together with the Metabolic Tracer Analysis Core (MTAC) facility at the University of Birmingham

Publications

T-cell metabolism governing activation, proliferation and differentiation; a modular view. Dimeloe S, Burgener AV, Grählert J, Hess C. Immunology. 2017 Jan;150(1):35-44 (Review Article) PMID: 27479920. http://onlinelibrary.wiley.com/doi/10.1111/imm.12655/full/

Memory CD8(+) T Cells Require Increased Concentrations of Acetate Induced by Stress for Optimal Function. Balmer ML, Ma EH, Bantug GR, Grählert J, Pfister S, Glatter T, Jauch A, Dimeloe S, Slack E, Dehio P, Krzyzaniak MA, King CG, Burgener AV, Fischer M, Develioglu L, Belle R, Recher M, Bonilla WV, Macpherson AJ, Hapfelmeier S, Jones RG, Hess C. Immunity. 2016 Jun 21;44(6):1312-24 PMID: 27212436 http://www.cell.com/immunity/fulltext/S1074-7613(16)30105-4

Targeting Metabolic Symbiosis to Overcome Resistance to Anti-angiogenic Therapy. Pisarsky L, Bill R, Fagiani E, Dimeloe S, Goosen RW, Hagmann J, Hess C, Christofori G. Cell Rep. 2016 May 10;15(6):1161-74. PMID: 27134168. http://www.cell.com/cell-reports/fulltext/S2211-1247(16)30441-7

 The Immune-Metabolic Basis of Effector Memory CD4+ T Cell Function under Hypoxic Conditions. Dimeloe S, Mehling M, Frick C, Loeliger J, Bantug GR, Sauder U, Fischer M, Belle R, Develioglu L, Tay S, Langenkamp A, Hess C. J Immunol. 2016 Jan 1;196(1):106-14 PMID: 26621861. http://www.jimmunol.org/content/196/1/106.long

Complement Regulates Nutrient Influx and Metabolic Reprogramming during Th1 Cell Responses. Kolev M, Dimeloe S, Le Friec G, Navarini A, Arbore G, Povoleri GA, Fischer M, Belle R, Loeliger J, Develioglu L, Bantug GR, Watson J, Couzi L, Afzali B, Lavender P, Hess C, Kemper C. Immunity. 2015 Jun 16;42(6):1033-47 PMID: 26084023. http://www.cell.com/immunity/fulltext/S1074-7613(15)00222-8

Human regulatory T cells lack the cyclophosphamide-extruding transporter ABCB1 and are more susceptible to cyclophosphamide-induced apoptosis. Dimeloe S, Frick C, Fischer M, Gubser PM, Razik L, Bantug GR, Ravon M, Langenkamp A, Hess C. Eur J Immunol. 2014 Dec;44(12):3614-20. PMID: 25251877. http://onlinelibrary.wiley.com/doi/10.1002/eji.201444879/full

Rapid effector function of memory CD8+ T cells requires an immediate-early glycolytic switch. Gubser PM, Bantug GR, Razik L, Fischer M, Dimeloe S, Hoenger G, Durovic B, Jauch A, Hess C. Nat Immunol. 2013 Oct;14(10):1064-72. PMID: 23955661. https://www.nature.com/articles/ni.2687

Defective IL-10 expression and in vitro steroid-induced IL-17A in paediatric severe therapy-resistant asthma. Gupta A, Dimeloe S, Richards DF, Chambers ES, Black C, Urry Z, Ryanna K, Xystrakis E, Bush A, Saglani S, Hawrylowicz CM. Thorax. 2014 Jun;69(6):508-15. PMID: 24347461. http://thorax.bmj.com/content/69/6/508.long

The role of 1α,25-dihydroxyvitamin D3 and cytokines in the promotion of distinct Foxp3+ and IL-10+ CD4+ T cells. Urry Z, Chambers ES, Xystrakis E, Dimeloe S, Richards DF, Gabryšová L, Christensen J, Gupta A, Saglani S, Bush A, O'Garra A, Brown Z, Hawrylowicz CM. Eur J Immunol. 2012 Oct;42(10):2697-708 PMID: 22903229. http://onlinelibrary.wiley.com/doi/10.1002/eji.201242370/full

 T cells producing the anti-inflammatory cytokine IL-10 regulate allergen-specific Th2 responses in human airways. Faith A, Singh N, Farooque S, Dimeloe S, Richards DF, Lu H, Roberts D, Chevretton E, Lee TH, Corrigan CJ, Hawrylowicz CM. Allergy. 2012 Aug;67(8):1007-13 PMID: 22671764. http://onlinelibrary.wiley.com/wol1/doi/10.1111/j.1398-9995.2012.02852.x/full

1α,25-dihydroxyvitamin D3 promotes CD200 expression by human peripheral and airway-resident T cells. Dimeloe S, Richards DF, Urry ZL, Gupta A, Stratigou V, Farooque S, Saglani S, Bush A, Hawrylowicz CM. Thorax. 2012 Jul;67(7):574-81. PMID: 22334534. http://thorax.bmj.com/content/67/7/574.long

Vitamin D binding protein and asthma severity in children. Gupta A, Dimeloe S, Richards DF, Bush A, Saglani S, Hawrylowicz CM. J Allergy Clin Immunol. 2012 Jun;129(6):1669-71 PMID: 22460073. http://www.jacionline.org/article/S0091-6749(12)00345-4/fulltext

Regulatory T cells, inflammation and the allergic response-The role of glucocorticoids and Vitamin D. Dimeloe S, Nanzer A, Ryanna K, Hawrylowicz C. J Steroid Biochem Mol Biol. 2010 May 31;120(2-3):86-95 (Review Article) PMID: 20227496. http://www.sciencedirect.com/science/article/pii/S096007601000083X?via%3Dihub

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