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Professor Sandra Sacre

Dr Sandra Sacre

Professor Sandra Sacre (PhD, PGCert, BSc)

Professor of Innate Immunity
T: +44 (0)1273 872865
Location: BSMS Medical Research Building, University of Sussex, Brighton, BN1 9PS

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

Other relevant positions: BSMS Early Career Research Lead

ResearchGate ID:
Loop profile:

Twitter: @ssacre



Sandra has worked at BSMS since November 2009. Her research strives to understand the regulation of innate immune signalling in both health and disease. She completed her undergraduate degree in Human Physiology followed by a PhD investigating the role of annexins in cardiovasular disease at University College London. Sandra then spent a year working on ApoE receptor signalling at the Royal Free Hospital in London before moving to the Kennedy Institute of Rheumatology at Imperial College London to work on toll-like receptors in rheumatoid arthritis. Sandra has continued working on rheumatoid arthritis at BSMS and expanded her research to include the autoimmune disease systemic lupus erythematosus. She was director of the Brighton Muscloskeletal Research Center from 2013-2017 and was a member of the British Society of Rheumatology Heberden Committee from 2016-2020. In 2014, Sandra was awarded the British Society of Rheumatology ‘Garrod Prize’ for her contribution to rheumatology. 


  • PhD, University College London, London, United Kingdom, 1 Jan 2000
  • BSc. Physiology, University College London, London, United Kingdom, 1 Jan 1993 - 1 Jan 1996
  • PGCert, University of Sussex, Brighton, United Kingdom, 2010-2012

Research interests

Innate immunity

Sandra's work focuses on understanding the innate immune system in health and disease. Innate immune cells express families of pattern recognition receptors that generate inflammation in response to viruses and bacteria but can also be activated by host molecules released at sites of inflammation and tissue damage. These receptors have an important role in defending again infections but in some people, they may also be responsible for unwanted inflammation present in autoimmune diseases. Much of Sandra’s work has focused on understanding a family of pattern recognition receptors called toll-like receptors and a multimeric complex termed the inflammasome. This research is performed in primary human monocytes and macrophages from healthy donors and patients with the autoimmune diseases’ rheumatoid arthritis and systemic lupus erythematosus. Understanding the contribution and regulation of innate immune receptors in specific disease settings, will aid the discovery of novel targets/approaches for future therapeutic interventions. 

The NLRP3 inflammasome

The inflammasome is a multimeric complex that is required for processing the inflammatory cytokines IL-1β and IL-18 before they are released from cells. There are several different types of inflammasome. In monocytes, the NLRP3 inflammasome performs this process following activation of toll-like receptors. Some research groups have suggested that the way the NLRP3 inflammasome is activated in monocytes is different to other cells. Much of this work has been performed in a transformed cell line that mimics human monocytes. Sandra’s group are currently working to confirm these findings in primary human monocytes and to understand further the molecular mechanisms regulating activation of the NLRP3 inflammasome. 

Toll-like receptors in Rheumatoid arthritis

Rheumatoid arthritis is an autoimmune disease characterised by chronic inflammation of the synovial joints leading to a progressive destruction of the joint architecture.  The inflammatory cytokines IL-1β, IL-6 and TNFβ have been demonstrated to have key roles in the disease process. Individually blocking the actions of these cytokines provides clinical benefit in some patients. Sandra’s research has previously demonstrated the potential for several toll-like receptors and their downstream signalling adaptor molecules MyD88 and MAL, to initiate the production of these cytokines from the synovial joint tissue of rheumatoid arthritis patients. Her research is currently focused on understanding how these receptors function in patient samples and how they are regulated at the molecular level.  

Toll-like receptors in Systemic lupus erythematosus (SLE)

SLE is a chronic systemic autoimmune disease, where a breakdown in immune tolerance 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.  Many studies have demonstrated the potential for members of the toll-like receptors family to contribute to the disease pathology. A major focus of Sandra’s current research is to understand how these receptors respond in patient samples and the molecular mechanisms regulating their activity. This work is currently funded by LUPUS UK. 

Teaching interests

Sandra is actively involved in teaching molecular cell biology and immunology within the curriculum at BSMS and is also an academic tutor. She is currently the module lead and the molecular cell biology theme lead for module 102: Foundations of health and disease. Sandra also teaches on module 204: Musculoskeletal and Immune Systems and the MSc. Internal Medicine. Her role also includes supervision of laboratory research projects for module 404, foundation year training academic rotations, undergraduate summer projects and PhD students.


TLR1/2 and 5 induce elevated cytokine levels from rheumatoid arthritis monocytes independent of ACPA or RF autoantibody status. Ryan S. Thwaites, Sarah Unterberger, Giselle Chamberlain, Karen Walker-Bone, Kevin. A. Davies & Sandra Sacre.  Rheumatology, 2020 (In Press).

Structural modification of the antidepressant mianserin reveals that its anti-inflammatory activity is independent of 5-hydroxytryptamine receptors. Sandra Sacre, Albert Jaxa-Chamiec, Caroline Low, Giselle Chamberlain, Cathy Tralau-Stewart. Front Immunol. 2019; May 24; 10:1167

Precipitation of Soluble Uric Acid is Necessary for in vitro Activation of the NLRP3 Inflammasome in Primary Human Monocytes. Alberts, Ben; Barber, James; Sacre, Sandra; Davies, Kevin; Ghezzi, Pietro; Mullen, Lisa.  J Rheumatol. 2019; 46 (9), 1141-1150

Oligodeoxynucleotide inhibition of Toll-like receptors 3, 7, 8 and 9 suppresses cytokine production in a human rheumatoid arthritis model. Sacre S., Lo A., Gregory B., Stephens M., Chamberlain G., Stott, P. and Brennan F. Eur J Immunol. 2016; Mar;46(3):772-781.

Simvastatin inhibits TLR8 signaling in primary human monocytes and spontaneous TNF production from rheumatoid synovial membrane cultures. Mullen L, Ferdjani J, Sacre S.  Mol Med. 2015; 21(1): 726–734. 

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

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

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

Inhibitors of toll-like receptor 8 reduce TNF production from human rheumatoid synovial membrane cultures. Sandra M. Sacre, Alexandra Lo, Bernard Gregory, Rachel Simmonds, Lynn Williams, Marc Feldmann, Fionula Brennan, and Brian M. Foxwell.  J. Immunol. 2008, 181:8002-9

The Toll-like receptor adaptor proteins MyD88 and Mal/TIRAP contribute to the inflammatory and destructive processes in a human model of rheumatoid arthritis. Sandra M. Sacre, Evangelos Andreakos, Serafim Kiriakidis, Parisa Amjadi, Anna Lundberg, Grey Giddins, Marc Feldmann, Fionula Brennan, and Brian M. Foxwell. American J. Pathol. 2007, 170 (2), 518-25.

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