Role of suppressor of cytokine signalling proteins in viral encephalitis

Research Opportunity
PhD students, Masters by Research, Honours students
Department / Centre
Microbiology and Immunology
Location
Doherty Institute
Primary Supervisor Email Number Webpage
Dr Lukasz Kedzierski lukaszk@unimelb.edu.au (03) 8344 0502 Personal web page
Co-supervisor Email Number Webpage
Professor John Fazakerley john.fazakerley@unimelb.edu.au (03) 9731 2261 Personal web page

Summary The suppressor of cytokine signalling (SOCS) proteins are key negative regulators of the JAK-STAT pathway and are responsible for controlling cytokine networks involved in immune response and inflammation. This project aims to explore the role of SOCS4 or SOCS5 during SFV induced encephalitis in a mouse model.

Project Details

The suppressor of cytokine signalling (SOCS) proteins are key negative regulators of the JAK-STAT pathway and are responsible for controlling cytokine networks involved in immune response and inflammation. SOCS are expressed in the central nervous system (CNS) and have the potential to modulate immune responses in the brain. We have recently shown that SOCS4- and SOCS5-deficient mice have different susceptibility phenotypes to an alphavirus infection, that virus RNA persists in the brain, and that infectious virus can be reactivated following immunosuppression. This project aims to explore the role of SOCS4 or SOCS5 during SFV induced encephalitis in a mouse model.



Faculty Research Themes

Infection and Immunology

School Research Themes

Infection & Immunity



Research Opportunities

PhD students, Masters by Research, Honours students
Students who are interested in joining this project will need to consider their elegibility as well as other requirements before contacting the supervisor of this research

Graduate Research application

Honours application

Key Contact

For further information about this research, please contact a supervisor.

Department / Centre

Microbiology and Immunology

Research Node

Doherty Institute

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