Toll and TLR function in inflammation and neurogenesis

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• Professor Nick Gay, Department of Biochemistry, Cambridge
• Wednesday 07 November 2012, 12:30-13:30
• Lecture Theatre, Department of Pathology, Tennis Court Road.

If you have a question about this talk, please contact Sue Griffin.

Host: Adrian Kelly (apk23@cam.ac.uk)

Although Drosophila Toll and vertebrate Toll-like receptors and their signalling pathways have a common evolutionary origin, the manner in which they recognise pathogen molecules is very different. The TLRs are bona fide pattern recognition receptors that directly bind a variety of microbial molecules. On the other hand immunity is mediated almost exclusively in Drosophila by the Toll1 receptor, which is activated by the endogenous cytokine Spatzle. What then is the function of the other 8 Drosophila Toll receptors? Our recent studies in collaboration with Alicia Hidalgo show that two of them Toll6 and 7, act as neurotrophin receptors in the insect central nervous system. Mutants lacking Toll6/7 have profound behavioural phenotypes and are activated by two Spatzle paralogues, DNT1 and DNT2 .

I will also discuss recent results concerning the specificity and regulation of the post receptor complexes, in particular the nature of TIR -TIR interactions between receptors and adaptors and the role of phosphorylation for the assembly and disassembly of Myddosomes.

This talk is part of the Immunology in Pathology series.

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