Skip to main contentSkip to footer
finger pointing scan
Brighton & Sussex Medical School

Staff Profiles

BSMS > About BSMS > Contact us > Staff > Dr Sandra Sacre

Dr Sandra Sacre


Dr Sandra Sacre (PhD, BSc)

Senior Lecturer in Molecular Cell Biology
T: +44 (0)1273 872865
Location: BSMS Medical Research Building, University of Sussex, Brighton, BN1 9PS

Other roles: Director of the Brighton Musculoskeletal Research Centre
Areas of expertise: Innate immune receptor signalling; inflammatory mechanisms in musculoskeletal diseases; primary human cell and tissue research
Research areas: Cell & developmental biology, infection & immunology, rheumatology


Dr Sandra Sacre completed her PhD investigating the role of annexins in cardiovasular disease  in 2000 at University College London. She then spent one year focusing on ApoE receptor signalling at the Royal Free Hospital in Hampstead before moving to the Kennedy Institute of Rheumatology (Imperial College London) to work on toll-like receptors (TLRs) in rheumatoid arthritis. In November 2009, Sandra moved to BSMS, where she continues to work on the role of TLRs in rheumatic diseases and is the Director of the Brighton Musculoskeletal Research Centre which she initiated in 2013. In 2014 Sandra was awarded the British Society of Rheumatology Garrod Prize for her contribution to research in rheumatic diseases.


Sandra's work focuses on the role of innate immune receptors that have an important function in the recognition of viruses and bacteria. These receptors are of particular interest in chronic inflammatory diseases as they can also generate cytokines in response to endogenous damage associated molecules often present at sites of inflammation and tissue damage. It is hoped that by increasing our understanding of the mechanisms by which the innate immune receptors contribute to inflammation in specific disease settings, it may be possible to identify novel targets/approaches for future therapeutic interventions.

Sandra's work focuses on three main disease areas:

Osteoarthritis (OA)

OA is the most common musculoskeletal complaint that leads to inflammation and the destruction of cartilage and bone causing disability and pain.

Rheumatoid arthritis (RA)

RA is primarily a disease of the joints but differs from OA in that it is an autoimmune disease generating much higher levels inflammation and cellular infiltration into the joint. In addition, systemic inflammation also affects other organs with a significant co-morbidity of cardiovascular disease and high prevalence of CNS effects, particularly fatigue and depression.

Systemic lupus erythamatosus (SLE)

SLE is a chronic systemic autoimmune disease, where a breakdown in tolerance within the immune system leads to sustained inflammation and tissue damage. Patients with SLE exhibit a diverse range of symptoms with multi-organ involvement that can include arthritis, nephritis, neuropsychiatric disturbances and dermatological complaints.


  • Leader of module 102: Foundations of health and disease
  • Theme leader for molecular cell biology
  • Lecturer in module 204: Musculoskeletal and Immune Systems
  • Module 404 Individual research Project Supervisor
  • Academic tutor
  • BSMS Exam boards for 102 and Phase 1
  • Chair of the Module 102 review board
  • F1/F2 academic rotation supervisor

Selected publications

Mullen L, Chamberlain G, Sacre S. Pattern recognition receptors as potential therapeutic targets in inflammatory rheumatic disease. Arthritis Res Ther. 2015;17(1).

Bryant C, Gay N, Heymans S, Sacre S, Schaefer L, Midwood K. Advances in Toll-like receptor biology: Modes of activation by diverse stimuli. Critical Reviews in Biochemistry and Molecular Biology. 2015;50(5):359-379.

Salzano S, Checconi P, Hanschmann E, Lillig C, Bowler L, Chan P et al. Linkage of inflammation and oxidative stress via release of glutathionylated peroxiredoxin-2, which acts as a danger signal. Proceedings of the National Academy of Sciences. 2014;111(33):12157-12162.

Thwaites R, Chamberlain G, Sacre S. Emerging Role of Endosomal Toll-Like Receptors in Rheumatoid Arthritis. Front Immunol. 2014;5.

Alzabin S, Kong P, Medghalchi M, Palfreeman A, Williams R, Sacre S. Investigation of the role of endosomal Toll-like receptors in murine collagen-induced arthritis reveals a potential role for TLR7 in disease maintenance. Arthritis Res Ther. 2012;14(3):R142.

Clanchy F, Sacre S. Modulation of toll-like receptor function has therapeutic potential in autoimmune disease. Expert Opinion on Biological Therapy. 2010;10(12):1703-1716.

Sacre S, Medghalchi M, Gregory B, Brennan F, Williams R. Fluoxetine and citalopram exhibit potent antiinflammatory activity in human and murine models of rheumatoid arthritis and inhibit toll-like receptors. Arthritis & Rheumatism. 2010;62(3):683-693.

Midwood K, Piccinini A, Sacre S. Targeting Toll-like Receptors in Autoimmunity. Current Drug Targets. 2009;10(11):1139-1155.

Midwood K, Sacre S, Piccinini A, Inglis J, Trebaul A, Chan E et al. Tenascin-C is an endogenous activator of Toll-like receptor 4 that is essential for maintaining inflammation in arthritic joint disease. Nature Medicine. 2009;15(7):774-780.