Sian Henson (0000-0003-1893-4912)

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Prof Henson is an immunologist interested in the mechanisms that drive T cell senescence. In particular, how changes to T cell metabolism during human ageing maintain an inflammatory deleterious state.
Her group at Queen Mary University of London has played a key role in highlighting the different metabolic requirements between CD4+ and CD8+ senescent T cells and have uncovered a novel role for the transcription factor GATA3 in the control of mitochondrial biogenesis. More recently, she has started to become interested in premature senescence phenotypes and their contribution to age-related disease.
She is the co-lead of the Life-long Health theme at QMUL, a multi-disciplinary effort to develop innovative research across the whole spectrum, from discovery science to health care services. She is also the lead for the CELLO network, CELLular metabolism Over a life-course in socioeconomic disadvantaged populations. The network is made up of researchers working in deprived places across the UK, and aims to address the impact of socioeconomic deprivation on healthy-life expectancy.

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Queen Mary University of London: London, GB

2022-09 to present | Professor of Immunology

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Sian Henson

https://orcid.org/0000-0003-1893-4912

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Biography

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Employment (7)

Queen Mary University of London: London, GB

Queen Mary University of London: London, London, GB

Queen Mary, University of London: London, GB

University College London: London, GB

University College London: London, GB

Imperial College London: London, London, GB

Chiltern International Ltd: Slough, Slough, GB

Education and qualifications (2)

Imperial College London: London, London, GB

University of Southampton: Southampton, Southampton, GB

Professional activities (10)

Biotechnology and Biological Sciences Research Council: Swindon, GB

British Society for Immunology: London, GB

Dunhill Medical Trust: London, GB

Frontiers in Immunology: London, GB

British Society for Research on Ageing: London, GB

British Society for Immunology: London, GB

Biotechnology and Biological Sciences Research Council: Swindon, GB

British Society for Immunology: London, GB

Strategic Promotion of Ageing Research Capacity : Reading, GB

British Society for Research on Ageing: London, GB

Funding (8)

Creation of CAR-Tregs that are resistant to the senescent environment

Metabolic intermediaries as drivers of inflammation and immunosenescence

Can the targeted removal of Tab1beta correct the function of senescent T cells from people living with type 2 diabetes

Understanding the role of inflammatory-derived senescent T cells during type 2 diabetes

Characterisation of metabolic dysfunction and altered T cell migration in lymphopenic perioperative individuals

Investigating the role of TAB1β a novel driver of senescence in type 2 diabetes

Investigating the dynamics of senescent human T-cell trafficking

Removing inflammation from senescent human T cells by targeting TAB1β, a novel driver of senescence.

Works (50 of 62)

The cellular senescence response and neuroinflammation in juvenile mice following controlled cortical impact and repetitive mild traumatic brain injury.

The generation of senescent-like CD4+ EMRA T cells in T2D and their contribution to poor COVID-19 vaccine responses

Senescent-like Blood Lymphocytes and Disease Progression in Amyotrophic Lateral Sclerosis

Metabolic requirements of Th17 cells and of B cells: Regulation and defects in health and in inflammatory diseases

The Expression of Active CD11b Monocytes in Blood and Disease Progression in Amyotrophic Lateral Sclerosis

Senescence and Type 2 Diabetic Cardiomyopathy: How Young Can You Die of Old Age?

Editorial: Targeting Leukocyte Trafficking: Insights and Future Directions.

Altered Nutrient Uptake Causes Mitochondrial Dysfunction in Senescent CD8+ EMRA T Cells During Type 2 Diabetes

Acute hyperglycaemic crisis after vaccination against COVID-19: A case series.

GATA3 induces mitochondrial biogenesis in primary human CD4<sup>+</sup> T cells during DNA damage.

Preoperative lymphopaenia, mortality, and morbidity after elective surgery: systematic review and meta-analysis.

Mitochondrial Dysfunction Accelerates Ageing.

Senescence and the Aging Immune System as Major Drivers of Chronic Kidney Disease.

Sequential interleukin 2 and pembrolizumab use in progressive multifocal leukoencephalopathy.

Immuno-metabolic impact of the multiple sclerosis patients' sera on endothelial cells of the blood-brain barrier.

Sestrins induce natural killer function in senescent-like CD8+ T cells.

Mitochondrial mass governs the extent of human T cell senescence

Pathogenic CD8+ Epidermis-Resident Memory T Cells Displace Dendritic Epidermal T Cells in Allergic Dermatitis.

Type 2 diabetes is associated with the accumulation of senescent T cells

Mitochondrial mass governs the extent of T cell senescence

Divergent mechanisms of metabolic dysfunction drive fibroblast and T-cell senescence

Skin resident memory CD8+ T cells are phenotypically and functionally distinct from circulating populations and lack immediate cytotoxic function

Human CD8+ EMRA T cells display a senescence-associated secretory phenotype regulated by p38 MAPK

Senescence of T Lymphocytes: Implications for Enhancing Human Immunity.

Killer Cell Lectin-like Receptor G1 Inhibits NK Cell Function through Activation of Adenosine 5'-Monophosphate-Activated Protein Kinase.

Killer Cell Lectin-like Receptor G1 Inhibits NK Cell Function through Activation of Adenosine 5′-Monophosphate–Activated Protein Kinase

Distinct Metabolic Requirements of Exhausted and Functional Virus-Specific CD8 T Cells in the Same Host.

CD8 + T-cell senescence: no role for mTOR

Blockade of PD-1 or p38 MAP kinase signaling enhances senescent human CD8(+) T-cell proliferation by distinct pathways.

Multifunctional cytomegalovirus (CMV)-specific CD8(+) T cells are not restricted by telomere-related senescence in young or old adults.

Genetic Regulation of Fate Decisions in Therapeutic T Cells to Enhance Tumor Protection and Memory Formation.

Defect in HSP90 expression in highly differentiated human CD8(+) T lymphocytes.

The Many Unknowns Concerning the Bioenergetics of Exhaustion and Senescence during Chronic Viral Infection.

The kinase p38 activated by the metabolic regulator AMPK and scaffold TAB1 drives the senescence of human T cells.

p38 signaling inhibits mTORC1-independent autophagy in senescent human CD8⁺ T cells.

IFN-α inhibits telomerase in human CD8⁺ T cells by both hTERT downregulation and induction of p38 MAPK signaling.

Age-associated increase of low-avidity cytomegalovirus-specific CD8+ T cells that re-express CD45RA.

The role of the T cell in age-related inflammation.

Differing HLA types influence inhibitory receptor signalling in CMV-specific CD8+ T cells.