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CALL FOR ABSTRACTS: TLRs (Toll-like receptors), NLRs (Nod-like proteins) and RLRs (RIG-like receptors), pathogens sensors of innate immunity

The Deadline for abstract submissions for oral presentation is July 10th 2009

Abstracts for poster presentation only can be submitted up to two weeks before the event

Please note that there will be a best poster prize.

All accepted abstracts will be published in the meeting proceedings

 

Date:  Friday, October 09, 2009 9:00 am - 5:00 pm


Venue:  BioPark Hertfordshire , United Kingdom

 

This meeting has CPD accreditation

 

 

 Chairs: Dr Martha Triantafilou/Dr Kathy Triantafilou, University of Sussex, UK

 

Talks include:         Immune recognition of fungal pathogens
Professor Neil A.R. Gow, University of Aberdeen, UK

Candida albicans is the most common agent of life-threatening human disease due to a fungus. We have constructed a series of mutant strains with alterations in C. albicans cell wall biosynthesis and used these to explore the role of the glycans on fungal pathogenesis.   Cytokine production by mononuclear cells or dendritic cells results from the detection of multiple wall components, singly and in combination. Other cell wall components block of shield the fungus from immune recognition by TLRs and lectin receptors. Therefore fungal recognition by the immune system is a complex and dynamic process triggered by multiple signals and multiple receptor complexes. [Reference:Netea, et al (2008) Nat Rev Microbiol 6, 67-78

 

Structure-function relationship of Toll-like receptor domains in different species and their potential impact on vaccine design

Professor Dirk Werling, Royal Veterinary College, UK

Toll-like receptors (TLRs) are a family of pattern recognition receptors that are an important link between innate and adaptive immunity. Many vaccines incorporate ligands for TLRs as an adjuvant and are developed in rodent models, with the resulting data transferred to other species. Vaccine features can be improved markedly by emphasizing the biological relevance when evaluating other animal models for host-pathogen interaction and by taking greater advantage of the unique experimental opportunities that are offered by large animal, non-rodent models. In the present talk, I will summarize our current knowledge of species-specific TLR responses and briefly discuss that vaccine efficacy in relevant host species might be improved by considering the species-specific TLR responses

 

RIG-like helicases and viral antagonists
Professor Steve Goodbourn, University of London, UK 
The RNA helicases, RIG-I and mda-5, recognise non-self RNA molecules generated in the cytoplasm, and signal through a common downstream adaptor to activate the transcription factors IRF-3 and NF-kappaB. These in turn signal the activation of an innate anti-viral program, including the production of type I interferon. In order to replicate efficiently, viruses must counter this system. This talk will focus on the mechanism of activation of RIG-I and mda-5 by viral RNAs, and their specific antagonism by viral proteins such as the paramyxovirus V protein and the influenza A virus NS1 protein.

 

Pattern recognition receptors and the host detection of bacterial infection

          Dr Clare Bryant, University of Cambridge, UK

Bacterial infection continues to cause major disease problems despite the availability of antibiotics.  We work on determining which Pattern Recognition Receptors (PRRs) detect important bacterial pathogens (specifically Salmonella enterica serovar Typhimurium and Streptococcus pneumoniae).  Lipopolysaccharide is a component of the Gram-negative bacterial cell wall and its detection by TLR4 and MD-2 drives protective immunity in the host.  We work on how TLR-4 and MD-2 detects lipid A structures and our comparative cross species analysis correctly predicted how the active TLR4/MD-2 signaling complex was formed.  This talk will focus on PRR recognition of Gram positive and Gram-negative bacteria.

 

 

See www.regonline.co.uk/TLR09 for more information, to register or to submit and abstract

 

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