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Professor Clare Bryant

Professor Clare Bryant

Clare Bryant is accepting applications for PhD students.

Clare Bryant is available for consultancy.

Research Interests

We study Pattern Recognition Receptors, such as Toll-like receptors (TLR), in different mammalian species studying their roles in responding to both purified bacterial ligands and infection with Salmonella entericia serovar Typhimurium (in collaboration with Duncan Maskell). We use gene arrays to study how bacterial gene expression changes in the phagosome of macrophages and use chimeric receptor constructs to study species-specific ligand interaction at the TLR4/MD2 complex (in collaboration with Nick Gay, Biochemistry). Currently we are studying the recruitment of adaptor proteins to TLR4, determining how S. Typhimurium bypasses the adaptor protein Mal during infection (in collaboration with Luke O’Neill, Dublin) and how S. Typhimurium activates the inflammasome. 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.


phagocytosis ; microarrays ; protein purification ; immunoprecipitation ; cell culture ; confocal microscopy ; interleukin ; cytokines ; reporter assays ; bacteria ; inflammation ; monocytes ; Toll-like receptors ; immunohistochemistry ; macrophages ; animal models ; pattern recognition receptors ; nitric oxide ; eicosanoids ; mutagenesis ; signal transduction ; innate immunity ; microscopy ; fluorescence microscopy ; signalling ; dendritic cells ; cloning


  • vaccines
  • cardiac immunity

Key Publications

Hepburn L, Prajsnar TK, Klapholz C, Moreno P, Loynes CA, Ogryzko NV, Brown K, Schiebler M, Hegyi K, Antrobus R, Hammond KL, Connolly J, Ochoa B, Bryant C, Otto M, Surewaard B, Seneviratne SL, Grogono DM, Cachat J, Ny T, Kaser A, Török ME, Peacock SJ, Holden M, Blundell T, Wang L, Ligoxygakis P, Minichiello L, Woods CG, Foster SJ, Renshaw SA, Floto RA. Innate immunity. A Spaetzle-like role for nerve growth factor β in vertebrate immunity to Staphylococcus aureus.
Science. 2014 Oct 31;346(6209):641-6.

Man SM, Hopkins LJ, Nugent E, Cox S, Glück IM, Tourlomousis P, Wright JA, Cicuta P, Monie TP, Bryant CE. Inflammasome activation causes dual recruitment of NLRC4 and NLRP3 to the same macromolecular complex. Proc Natl Acad Sci U S A. 2014 May 6

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. Allergens as Immunomodulatory Proteins: The Cat Dander Protein Fel d 1 Enhances TLR Activation by Lipid Ligands. J Immunol. 2013 Aug 15;191(4):1529-35.

Bryant CE, Monie TP. Mice, men and the relatives: cross-species studies underpin innate immunity. Open Biol. 2012 Apr;2(4):120015.

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. Dynamics of Salmonella infection of macrophages at the single cell level. J R Soc Interface. 2012 Oct 7;9(75):2696-707

Smyth T, Tötemeyer S, Haugland S, Willers C, Peters S, Maskell D, and Bryant CE, (2008) Dexamethasone modulates Salmonella entericia serovar Typhimurium infection in vivo independently of the glucocorticoid-inducible protein annexin 1, FEMS Immunol. Micro. (In press; available on line).

Núñez Miguel R, Wong J, Westoll JF, Brooks HJ, O’Neill LAJ, Gay NJ, Bryant CE, and Monie TP, (2007) A Dimer of the Toll-Like Receptor 4 Cytoplasmic Domain Provides a Specific Scaffold for the Recruitment of Signalling Adaptor Proteins. PLoS One 2, e788.

Tötemeyer S, Sheppard S, Lloyd A, Roper D, Dowson C, Underhill D, Murray P, Maskell D, Bryant, C.E (2006) Interferon-gamma enhances production of nitric oxide from macrophages via a mechanism that depends on NOD 2, J. Immunol. 176, 4804–10

Tötemeyer S, Kaiser P, Maskell DJ, Bryant CE, (2005) Sublethal infection of C57BL/6 mice with Salmonella enterica serovar Typhimurium leads to an increase in levels of Toll-like receptor 1 (TLR1), TLR2, and TLR9 mRNA as well as a decrease in levels of TLR6 mRNA in infected organs. Infect. Immun. 73,1873–8