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TLRs (Toll-like receptors), NLRs (Nod-like proteins) and RLRs (RIG-like receptors), pathogens sensors of innate immunity – 9th October 2009

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  • UserThe meeting chairs are Dr Martha Triantafilou and Dr Kathy Triantafilou, speakers are Professor Neil A.R. Gow,Professor Dirk Werling,. Professor Steve Goodbourn,Dr Helen S Atkins,. Dr Clare Bryant, Dr Nick Gay,Dr Olaf Gross,Dr Tom Monie
  • ClockFriday 09 October 2009, 09:00-17:00
  • HouseThe BioPark, Hertfordshire,AL7 3AX UK.

If you have a question about this talk, please contact Speaker to be confirmed.

“Significant advances in our understanding of the innate immune recognition have been made in the last decade following the identification of three families of pattern recognition receptors: Toll-like receptors (TLRs), NOD -like receptors (NLRs) and RIG -I-like receptors (RLRs). TLRs are pattern recognition receptors that detect motifs or signatures from bacteria, viruses, protozoa and fungi. NLRs detect mainly intracellular bacteria and RLRs detect viral genome. These three families of pattern recognition receptors comprise the front line of defence that the host possesses against microbial pathogens. The aim of this meeting is to provide an overview of these three families of receptors and provide the most recent advances in the area of innate immune pattern recognition”. Chairs: Dr Martha Triantafilou/Dr Kathy Triantafilou, University of Sussex, UK

The agenda includes: 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.

Dr Helen S Atkins, Defence Science and Technology Laboratory, Porton Down, UK – talk to be confirmed

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.

Pathogen pattern rocognition by Toll-like receptors – 20 years on .Dr Nick Gay, University of Cambridge, UK In my talk I will describe the molecular mechanisms by which these conserved pathogen associated moecules are recognized by the TLRs with particular reference to lipo polysaccharide and single stranded viral RNAs. I will also present new results which show how receptor activation is coupled to downstream signal transduction and in particular the role played by oligomeric signaling platforms assembled form adaptors and other signaling molecules involved in the pathway. I will discuss the potential for structural analysis to be used in the rational design of new drugs.

ITAM -coupled receptor signaling and the Nalp3-inflammasome in anti-fungal immunity. Dr Olaf Gross, University of Lausanne, Switzerland

CARD tricks – more than just a magic show. Dr Tom Monie, Wellcome Trust Career Development Fellow , Cambridge Homotypic interactions between the effector domains of NLR proteins are essential for the propagation of signal transduction and the activation of the inflammasome. This talk will discuss the mechanisms by which these interactions are mediated with a particular focus on the caspase activation and recruitment domain (CARD):CARD interactions of NOD1 and its signalling partner the serine/threonine kinase RIP2 .

The Deadline for early registration is July 20th 2009. After this time the fees double, so make sure you book early!

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

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