CANCELLED Salmonella Employs a Kinase Converting Effector to Drive Macrophage Polarisation
4:00pm - 5:00pm /
Tuesday 19th November 2019
/ Venue: LT2 Life Sciences Building
- Jay Hinton
- Suitable for: Staff and students with an interest in Behaviour, Evolution, Ecology and Microbiology
- Admission: Free
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Speaker: Teresa Thurston (Imperial College London)
Bacterial infections often cause significant health problems and even death in humans. The host innate immune response provides a first line of defence against pathogens and is essential for inducing adaptive immunity and ultimately, pathogen clearance. However, many Gram-negative bacterial pathogens antagonize anti-bacterial immunity through translocated effector proteins that inhibit pro-inflammatory signaling. The Salmonella effector SteE drives STAT3 activation, polarising macrophages to an anti-inflammatory M2 phenotype, thereby creating a favourable intracellular niche for the pathogen. We have recently found that SteE forces a switch in the amino acid and substrate specificity of the host kinase GSK3. The conversion of this pleiotropic serine/threonine kinase into a tyrosine kinase represents an unprecedented example of how a bacterial virulence protein reprograms innate immune signaling to establish an anti-inflammatory environment.
Bacterial infections often cause significant health problems and even death in humans. The host innate immune response provides a first line of defence against pathogens and is essential for inducing adaptive immunity and ultimately, pathogen clearance. However, many Gram-negative bacterial pathogens antagonize anti-bacterial immunity through translocated effector proteins that inhibit pro-inflammatory signaling. The Salmonella effector SteE drives STAT3 activation, polarising macrophages to an anti-inflammatory M2 phenotype, thereby creating a favourable intracellular niche for the pathogen. We have recently found that SteE forces a switch in the amino acid and substrate specificity of the host kinase GSK3. The conversion of this pleiotropic serine/threonine kinase into a tyrosine kinase represents an unprecedented example of how a bacterial virulence protein reprograms innate immune signaling to establish an anti-inflammatory environment.