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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 rheumatic diseases; primary human cell and tissue research and neuroinflammation.

Research areas: Inflammatory disease & immunity; neuroscience

Other relevant positions: BSMS Director of Doctoral Studies. British Society for Immunology Congress Committee. Associate Editor Frontiers in Immunology.

ResearchGate ID:
Loop profile:

Twitter: @ssacre



Sandra is a Professor of Innate Immunity at BSMS, where her research strives to understand the innate immune system and how it is regulated in health and disease. She studied human physiology at University College London, followed by a PhD investigating the role of annexins in cardiovascular disease. Sandra then 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 investigate the role of toll-like receptors in rheumatoid arthritis. 

In 2009 Sandra joined BSMS, where she continues working on rheumatic diseases focused on rheumatoid arthritis and lupus, alongside projects expanding the knowledge of innate immune regulation in health and the mechanisms underlying neuroinflammation in Alzheimer’s Disease.  In 2014, Sandra was awarded the British Society of Rheumatology ‘Garrod Prize’ for her contribution to rheumatology. In addition to her research and teaching roles, Sandra was director of the Brighton Musculoskeletal Research Centre from 2013-2017 and was a member of the British Society of Rheumatology Heberden Committee from 2016-2020. Sandra is currently the Director of Doctoral Studies at BSMS and a member of the British Society for Immunology congress committee. 


  • 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

Our research projects focus on understanding the innate immune system in health and disease. Innate immune cells express pattern recognition receptors that produce 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 are responsible for unwanted inflammation associated with autoimmune and neurodegenerative diseases. Much of our work has focused on a family of pattern recognition receptors called toll-like receptors and a multi-protein complex termed the inflammasome. 

This research is mainly performed in primary human monocytes/macrophages from healthy donors and tissue relevant cell types from patients with inflammatory diseases. Understanding the contribution and regulation of innate immune receptors and their signalling pathways in specific disease settings, is an important foundation for the discovery of novel targets for therapeutic approaches in the future.  

The NLRP3 inflammasome

NLRP3 is part of the family of NOD-like receptor (NLR) proteins, which are pattern recognition receptors found in the cytoplasm of immune cells. It is a sensor of danger that forms a multi-protein complex called an inflammasome, to process the inflammatory cytokines IL-1β and IL-18 before they are released from cells. The inflammasome can be activated by different cellular pathways depending on the cell type and location of the danger signal; they are termed the canonical, non-canonical and alternative pathways. Researchers have shown that in human monocytes, the NLRP3 inflammasome can be activated by the alternative pathway following activation of toll-like receptor 4.

The activation of the NLRP3 inflammasome is tightly regulated to avoid excessive or prolonged inflammation, as this can lead to tissue damage and contribute to the pathogenesis of several inflammatory diseases. Our research has demonstrated that SARM1, a regulator of the NLRP3 inflammasome, is itself dysregulated and expressed at lower levels in patients with active rheumatoid arthritis. 

Our current projects focus on exploring the molecular mechanism of NLRP3 inflammasome activation in primary human monocytes and the role of the NLRP3 inflammasome in neuroinflammation associated with Alzheimer’s Disease.  

Toll-like receptors (TLRs)

TLRs are a key component of the immune system's ability to detect invading pathogens, such as bacteria and viruses, as well as recognising endogenous molecules released during tissue damage or cellular stress. These molecular patterns associated with pathogens or tissue damage are referred to as pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs), respectively. 

While TLRs play a crucial role in detecting pathogens and initiating the immune response, dysregulation of TLR signalling has been associated with chronic inflammatory diseases and autoimmune conditions. Understanding the function and regulation of toll-like receptors has significant importance for the development of therapies and vaccines targeting infectious diseases and inflammatory disorders.

We have previously demonstrated the potential for several members of the toll-like receptor family and their downstream signalling adaptor molecules to initiate the production of pro-inflammatory cytokines within the synovial joint tissue of rheumatoid arthritis patients. Furthermore, we have shown that some TLRs generate higher levels of cytokines from peripheral blood monocytes in these patients which was not linked to their autoantibody status. 

Our current projects have extended these finding to explore the role of these receptors and how they are regulated in systemic lupus erythematosus.

Anti-Microbial Peptides

Host defence peptides (HDPs) are an essential part of the innate immune system forming one of the first lines of defence again pathogens. There are several different families of HDPs. Humans only express one member of the cathelicidin family of HDPs, LL-37 a short 37aa amphipathic peptide produced by proteolytic cleavage of the protein hCAP18. LL-37 is released by several cell types including barrier epithelial cells, as well as monocytes, macrophages, and neutrophils at sites of infection. It is best known for its roles in bacterial cell lysis, viral neuralisation and ability to directly bind and inhibit lipopolysaccharide on Gram-negative bacteria. However, novel immunomodulatory roles for LL-37 are now emerging. 

Our current research explores the functional effect of LL-37 on human monocyte to enable us to better understand its role at sites of inflammation. 

Lab members

Current members

Flora Bertwistle
Lucy MacAleese 

Past members

Dr Ryan Thwaites
Dr Sarah Unterberger
Dr Giselle Chamberlain
Dr Lisa Mullen
Dr Kaj Kreutzfeldt
Dr Laura Whitely
Dr Matthew Stephens


Prof Louise Serpell, University of Sussex, UK
Dr Ben Towler, University of Sussex, UK
Prof Naji Tabet, Brighton and Sussex Medical School, UK
Prof Rachel Simmonds, University of Surrey, UK
Dr Emily Gwyer Findlay, University of Southampton, UK  
Dr Sanna Palosaari, University of Oulu, Finland   


Sandra is actively involved in teaching molecular cell biology and immunology within the curriculum at BSMS. She is currently 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.


The One That Got Away: How Macrophage-Derived IL-1β Escapes the Mycolactone-Dependent Sec61 Blockade in Buruli Ulcer. Hall BS, Hsieh LT, Sacre S, Simmonds RE. Front Immunol. 2022 Jan 26;12:788146. doi: 10.3389/fimmu.2021.788146. eCollection 2021.

Expression of sterile-α and armadillo motif containing protein (SARM) in rheumatoid arthritis monocytes correlates with TLR2-induced IL-1β and disease activity. Thwaites RS, Unterberger S, Chamberlain G, Gray H, Jordan K, Davies KA, Harrison NA, Sacre S. Rheumatology (Oxford). 2021 Dec 1;60(12):5843-5853. doi: 10.1093/rheumatology/keab162.

Contribution of Toll-Like Receptors and the NLRP3 Inflammasome in Rheumatoid Arthritis Pathophysiology. Unterberger S, Davies KA, Rambhatla SB, Sacre S. Immunotargets Ther. 2021 Jul 28;10:285-298. doi: 10.2147/ITT.S288547. eCollection 2021. 

Clanchy FIL, Borghese F, Bystrom J, Balog A, Penn H, Hull DN, Wells GMA, Kiriakidis S, Taylor PC, Sacre SM, Williams LM, Stone TW, Mageed RA, Williams RO. TLR expression profiles are a function of disease status in rheumatoid arthritis and experimental arthritis. J Autoimmun. 2021 Mar;118:102597. doi: 10.1016/j.jaut.2021.102597. 

TLR1/2 and 5 induce elevated cytokine levels from rheumatoid arthritis monocytes independent of ACPA or RF autoantibody status. Thwaites RS, Unterberger S, Chamberlain G, Walker-Bone K, Davies KA, Sacre S. Rheumatology (Oxford). 2020 Nov 1;59(11):3533-3539. doi: 10.1093/rheumatology/keaa220. 

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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