Professor of Innate Immunity
Departmental Research Director
Pattern Recognition Receptors
Clare Bryant is interested in taking PhD students.
Clare Bryant is available for consultancy.
Clare graduated in biochemistry before training as a vet in London. She was funded by the Wellcome Trust for her PhD (in London) before moving to the William Harvey Research Institute for 4 years as a Wellcome postdoctoral fellow. She then moved to Cambridge as a Wellcome Trust Career Development Fellow where she is now Professor of Innate Immunity.
Subject groups/Research projects
- Infection and Immunity:
Pattern Recognition Receptor biology, innate immunity, Salmonella infection biology, imaging
Departments and Institutes
We use multidisciplinary approaches to understand how bacteria are detected by the host (through Pattern Recognition Receptors (PRRs)) and how pathogen detection links to inflammatory diseases such as allergies. The host has many Pattern Recognition Receptors (PRRs), such as Toll-like receptors (TLRs) and Nod-like receptors (NLRs), that detect bacteria, such as Salmonella entericia serovar Typhimurium, and their associated molecules (such as endotoxin). We are studying which PRRs detect S. Typhimurium to drive an adaptive immune responses focussing on the NLRs and their effector mechanisms. We work with Pietro Cicuta (Physics), Julia Gog (DAMPT) and Ray Goldstein (DAMPT) to study bacterial interactions with cells and respiratory tissues using mathematical modelling, optical tweezers and real-time imaging.
We are studying the molecular mechanisms underlying how ligands, such as endotoxin, interact with TLR4/MD2 receptor complex to recruit their adaptor signalling molecules, such as Mal and Tram, to initiate intracellular signalling (in collaboration with Nick Gay, Biochemistry). We are using FRET analysis and single molecule florescence techniques to study how TLRs form active signalling protein complexes and recruit adaptor proteins in real-time in live cells (in collaboration with David Klenerman, Chemistry).
Allergens, such as the cat dander protein Fel D1, are readily contaminated by endotoxin and this allows them to be detected by TLR4. Prevention of host detection may prevent the onset of an allergic response. In particular we are interested in how allergens, such as the cat dander protein Fel d1 enhances TLR4 signalling and whether we can design inhibitors to prvent allergen recognition.
Our work is funded by the Wellcome Trust, the MRC, the BBSRC and the HBLB.
Main collaborators Live imaging of Salmonella infecting a macrophage
- Ray Goldstein, DAMPT, Cambridge
- Julia Gog, DAMPT, Cambridge
- Pietro Cicuta, Physics, Cambridge
- David Spring, Department of Chemistry, Cambridge
- David Klenerman, Department of Chemistry, Cambridge
- Kate Fitzgerald, UMass Medical School, Worcester, USA
- Doug Golenbock, UMass Medical School, Worcester, USA
- Luke O'Neill, Trinity College, Dublin, Ireland
- Michael White, University of Liverpool
- Man, S.M., Hopkins,L.J., Nugent, E., Cox, S., Glück, I., Tourlomousis, P., Wright, J.A., Cicuta, P., Monie, T.P. and Bryant, C.E. (2014)Inflammasome activation causes dual recruitment of NLRC4 and NLRP3 to the same macro-molecular complex. Proc Natl Acad Sci
Man SM, Tourlomousis P, Hopkins L, Monie TP, Fitzgerald KA, Bryant CE. "Salmonella Infection Induces Recruitment of Caspase-8 to the Inflammasome To Modulate IL-1β Production".(2013) J Immunol. 191(10):5239-46.[PubMed]
Herre J, Grönlund H, Brooks H, Hopkins L, Waggoner L, Murton B, Gangloff M, Opaleye O, Chilvers ER, Fitzgerald K, Gay N, Monie T, Bryant C. (2013) "Allergens as immunomodulatory proteins: the cat dander protein Fel d 1 enhances TLR activation by lipid ligands". J Immunol. 191(4):1529-35.[PubMed}
Gog JR, Murcia A, Osterman N, Restif O, McKinley TJ, Sheppard M, Achouri S, Wei B, Mastroeni P, Wood JL, Maskell DJ, Cicuta P, Bryant CE (2012). “Dynamics of Salmonella infection of macrophages at the single cell level” J R Soc Interface 9(75):2696-707
- Bryant, C. E., D. R. Spring, M. Gangloff and N. J. Gay (2010) "The molecular basis of the host response to lipopolysaccharide." Nat Rev Microbiol 8(1): 8-14. [PubMed]
- Bryant, C. and K. A. Fitzgerald (2009). "Molecular mechanisms involved in inflammasome activation." Trends Cell Biol 19(9): 455-64. [PubMed]
- Talbot, S., S. Totemeyer, M. Yamamoto, S. Akira, K. Hughes, D. Gray, T. Barr, P. Mastroeni, D. J. Maskell and C. E. Bryant (2009). "Toll-like receptor 4 signalling through MyD88 is essential to control Salmonella enterica serovar typhimurium infection, but not for the initiation of bacterial clearance." Immunology 128(4): 472-83. [PubMed]
- Wright, J. A., S. S. Totemeyer, I. Hautefort, C. Appia-Ayme, M. Alston, V. Danino, G. K. Paterson, P. Mastroeni, N. Menager, M. Rolfe, A. Thompson, S. Ugrinovic, L. Sait, T. Humphrey, H. Northen, S. E. Peters, D. J. Maskell, J. C. Hinton and C. E. Bryant (2009). "Multiple redundant stress resistance mechanisms are induced in Salmonella enterica serovar Typhimurium in response to alteration of the intracellular environment via TLR4 signalling." Microbiology 155(Pt 9): 2919-29. [PubMed]
- Walsh, C., M. Gangloff, T. Monie, T. Smyth, B. Wei, T. J. McKinley, D. Maskell, N. Gay and C. Bryant (2008). "Elucidation of the MD-2/TLR4 interface required for signaling by lipid IVa." J Immunol 181(2): 1245-54. [PubMed]