Imperial College London


Faculty of MedicineDepartment of Infectious Disease

Research Fellow



+44 (0)20 7594 3072t.thurston




2.40Flowers buildingSouth Kensington Campus





Research Summary

Research in the Thurston laboratory seeks to understand what determines the fate of intracellular bacteria, a complex interaction mediated by both the host and the pathogen. On the host side, our research focuses on cell-intrinsic innate immune mechanisms that protect against intracellular bacteria. To complement this, our other area of research focuses on how Salmonella effector proteins, delivered into host cells, manipulate innate immune signaling.



Teresa completed her PhD in 2010 with Dr. Felix Randow, at the Laboratory of Molecular Biology, University of Cambridge. During this time and a short postdoc period, she worked on understanding how antibacterial autophagy functions as a cell autonomous innate immune mechanism to restrict the growth of cytosolic bacteria.

In 2011, Teresa joined the CMBI as a postdoc in the laboratory of Prof. David Holden, focusing on Salmonella as a model intracellular pathogen. She was awarded an Early Career Research Fellowship from the Leverhulme Trust in 2012 and an Imperial College Research Fellowship in 2014 to establish her own research focused on innate immune signaling during Salmonella infection. 

In July 2018 Teresa took up a 5 year BBSRC David Phillips Fellowship within the CMBI to continue investigating host-pathogen interactions. The goal of this research is to use a multidisciplinary approach encompassing proteomics, genetic screens, cell biology and structural biology, to identify and investigate how both host and pathogen determinants alter the outcome of bacterial infections. Such fundamental research into understanding host-pathogen interactions is needed to provide valuable insight into the pathophysiology of bacterial infections and represents an essential step for future research into novel therapeutic strategies.



Panagi I, Jennings E, Zeng J, et al., 2020, Salmonella effector SteE converts the mammalian serine/threonine kinase GSK3 into a tyrosine kinase to direct macrophage polarization., Cell Host and Microbe, Vol:27, ISSN:1931-3128, Pages:41-53.e6

Pham THM, Brewer SM, Thurston T, et al., 2020, Salmonella-driven polarization of granuloma macrophages antagonizes TNF-mediated pathogen restriction during persistent infection, Cell Host and Microbe, Vol:27, ISSN:1931-3128, Pages:54-67.E5

Panagi I, Jennings E, Zeng J, et al., The <i>Salmonella</i> Effector SteE Converts the Mammalian Serine/Threonine Kinase GSK3 into a Tyrosine Kinase, Cell Host and Microbe, ISSN:1931-3128

Stapels DAC, Hill PWS, Westermann AJ, et al., 2018, Salmonella persisters undermine host immune defenses during antibiotic treatment, Science, Vol:362, ISSN:0036-8075, Pages:1156-1160

Jennings E, Esposito D, Rittinger K, et al., 2018, Structure-function analyses of the bacterial zinc metalloprotease effector protein GtgA uncover key residues required for deactivating NF-B, Journal of Biological Chemistry, Vol:293, ISSN:0021-9258, Pages:15316-15329

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