Professor Sian Henson

Profile

ORCID iD: 0000-0003-1893-4912

Sian Henson obtained her PhD at Imperial College London in 2000. Subsequently, Sian undertook postdoctoral training with Prof Richard Aspinall at Imperial College investigating the role of IL-7 in thymic atrophy. She then moved to Prof Arne Akbar’s lab at University College London where she directed her focus towards understanding the role of inhibitory receptors during ageing and found that senescence is not passive end-stage processes but is controlled by active signalling pathways. More recently she has become interested in the metabolic requirements of primary human senescent T cells. Sian became a lecturer at the William Harvey Research Institute in 2015 where she has established her own research group investigating the deregulation of T cell metabolism during human ageing and how it maintains an inflammatory deleterious state.  

Professor Henson serves as a committee member for the BBSRC and the Dunhill Medical Trust. She is the Chair of the British Society of Immunology affinity group for Immune senescence. Sian is also an Associate Editor for Frontiers of Immunology. Current academic roles include module lead for Immunology for the Biomedical Sciences BSc.

Research

Group members

• Johannes Schroth
• Conor Garrod-Ketchley

Summary 

Ageing is accompanied by alterations to T cell immunity and by a low-grade chronic inflammatory state, termed inflammaging. Although inflammation is critical for dealing with infections and tissue damage, inflammaging appears to be physiologically deleterious and predictive of all-cause mortality in multiple elderly cohorts. The maintenance of this inflammatory state is mediated by metabolic changes. Immune metabolism is an emerging field of research with little information regarding the metabolism and metabolic checkpoints that regulate T cell ageing. The aim of my work is to investigating how changes to T cell metabolism during human ageing maintains this inflammatory state.  

Senescent CD8+ T cell displaying dysfunctional ‘giant’ mitochondria, which contribute to the bioenergetic instability of these cells. 

Publications

Collaborators