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Does subversion of Toll-like receptor signalling play a role in directing TH2 responses by the filarial nematode secreted product ES-62?

Reference	S17074
Principal Investigator / Supervisor	Professor Margaret Harnett
Co-Investigators / Co-Supervisors	Dr Helen Goodridge, Professor William Harnett, Professor Foo Liew
Institution	University of Glasgow
Department	Immunology & Bacteriology
Funding type	Research
Value (£)	174,368
Status	Completed
Type	Research Grant
Start date	01/04/2002
End date	01/04/2005
Duration	36 months

Abstract

ES-62, an immunomodulatory, phosphorylcholine-containing glycoprotein secreted by filarial nematodes biases the T cell immune response towards TH2, an anti-inflammatory phenotype that promotes parasite survival. ES-62 induces this polarisation both by suppressing the production of IL-12, a key cytokine in the development of TH1:inflammatory responses, from macrophages and inducing the development of a dendritic cell phenotype that initiates TH2 responses. Macrophage and dendritic cell function can be driven by Toll-Like Receptor (TLR) signalling and our recent data suggest that ES-62 binds to and signals via TLRs on target cells. The core aim of this project is therefore to define whether subversion of TLRs transduces the signals by which ES-62 initiates TH2:anti-inflammatory responses and or reverses the polarity of ongoing TH1 responses.

Summary

unavailable

Committee	Closed Committee - Animal Sciences (AS)
Research Topics	X – not assigned to a current Research Topic
Research Priority	X – Research Priority information not available
Research Initiative	X - not in an Initiative
Funding Scheme	X – not Funded via a specific Funding Scheme

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