Communications Biology (Oct 2021)
Therapeutically expanded human regulatory T-cells are super-suppressive due to HIF1A induced expression of CD73
- Lorna B. Jarvis,
- Daniel B. Rainbow,
- Valerie Coppard,
- Sarah K. Howlett,
- Zoya Georgieva,
- Jessica L. Davies,
- Harpreet Kaur Mullay,
- Joanna Hester,
- Tom Ashmore,
- Aletta Van Den Bosch,
- James T. Grist,
- Alasdair J. Coles,
- Hani S. Mousa,
- Stefano Pluchino,
- Krishnaa T. Mahbubani,
- Julian L. Griffin,
- Kourosh Saeb-Parsy,
- Fadi Issa,
- Luca Peruzzotti-Jametti,
- Linda S. Wicker,
- Joanne L. Jones
Affiliations
- Lorna B. Jarvis
- Department of Clinical Neurosciences, University of Cambridge
- Daniel B. Rainbow
- Department of Clinical Neurosciences, University of Cambridge
- Valerie Coppard
- Department of Medicine, University of Cambridge
- Sarah K. Howlett
- Department of Clinical Neurosciences, University of Cambridge
- Zoya Georgieva
- Department of Clinical Neurosciences, University of Cambridge
- Jessica L. Davies
- Department of Clinical Neurosciences, University of Cambridge
- Harpreet Kaur Mullay
- Department of Clinical Neurosciences, University of Cambridge
- Joanna Hester
- Department of Nuffield Department of Surgical Sciences, University of Oxford
- Tom Ashmore
- Department of Biochemistry and Cambridge Systems Biology Centre, University of Cambridge
- Aletta Van Den Bosch
- Department of Clinical Neurosciences, University of Cambridge
- James T. Grist
- Department of Radiology, University of Cambridge
- Alasdair J. Coles
- Department of Clinical Neurosciences, University of Cambridge
- Hani S. Mousa
- Department of Clinical Neurosciences, University of Cambridge
- Stefano Pluchino
- Department of Clinical Neurosciences, University of Cambridge
- Krishnaa T. Mahbubani
- Department of Surgery, University of Cambridge
- Julian L. Griffin
- Department of Biochemistry and Cambridge Systems Biology Centre, University of Cambridge
- Kourosh Saeb-Parsy
- Department of Surgery, University of Cambridge
- Fadi Issa
- Department of Nuffield Department of Surgical Sciences, University of Oxford
- Luca Peruzzotti-Jametti
- Department of Clinical Neurosciences, University of Cambridge
- Linda S. Wicker
- JDRF/Wellcome Diabetes and Inflammation Laboratory, Wellcome Centre for Human Genetics, Nuffield Department of Medicine, NIHR Oxford Biomedical Research Centre, University of Oxford
- Joanne L. Jones
- Department of Clinical Neurosciences, University of Cambridge
- DOI
- https://doi.org/10.1038/s42003-021-02721-x
- Journal volume & issue
-
Vol. 4,
no. 1
pp. 1 – 14
Abstract
Jarvis et al demonstrate that expanded human Tregs switch their metabolism to aerobic glycolysis and show enhanced suppressive function through hypoxia-inducible factor 1-alpha (HIF1A)-driven acquisition of CD73 expression, which along with CD39, enables expanded Tregs to convert ATP to immunosuppressive adenosine. Given this, the data suggests that Treg expansion protocols should be optimised for CD39/CD73 co-expression to enhance therapeutic potential.
