Dionne: Difference between revisions
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That is to say, Marc Dionne's lab, at King's College London; not to be confused with any other Dionne lab. | That is to say, Marc Dionne's lab, at King's College London; not to be confused with any other Dionne lab. | ||
We are interested in (1) the effects of host genetics on the biology of infection; and (2) | We are interested in (1) the effects of host genetics on the biology of infection; and (2) cytokine signalling and its effects on immune and non-immune tissues. ''Drosophila melanogaster'' is our animal model of choice. | ||
Work in the lab is funded by [http://bbsrc.ac.uk the Biotechnology and Biological Sciences Research Council]. | Work in the lab is funded by [http://www.bbsrc.ac.uk the Biotechnology and Biological Sciences Research Council] and [http://www.wellcome.ac.uk the Wellcome Trust]. | ||
==We've moved!== | |||
The lab has moved from its original digs (on the 27th and 28th floors of Guy's Tower) across the street to New Hunt's House in order to be part of the new Centre for the Molecular and Cellular Biology of Inflammation. Our academic affiliation will be changing to the Peter Gorer Department of Immunobiology, DIIID, School of Medicine. Directions and postal addresses have been corrected on the [http://dionne.openwetware.org/Contact.html Contact] page. | |||
==Host genetics and the biology of infection== | ==Host genetics and the biology of infection== | ||
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So far, our work on this system has focused on the mechanisms of pathogenesis. We have found that this infection causes progressive loss of metabolic stores, similar to the wasting seen in people with tuberculosis. We have shown that, in the fly, this wasting effect is caused partly by systemic failures in anabolic signals via the insulin effector kinase Akt. We are now working to try to understand how infection causes this defect in anabolic signalling. We also have mutants that affect other aspects of disease; we are working with these mutants to understand other aspects of disease pathogenesis as well as how the fly immune system fights Mycobacterial infections. | So far, our work on this system has focused on the mechanisms of pathogenesis. We have found that this infection causes progressive loss of metabolic stores, similar to the wasting seen in people with tuberculosis. We have shown that, in the fly, this wasting effect is caused partly by systemic failures in anabolic signals via the insulin effector kinase Akt. We are now working to try to understand how infection causes this defect in anabolic signalling. We also have mutants that affect other aspects of disease; we are working with these mutants to understand other aspects of disease pathogenesis as well as how the fly immune system fights Mycobacterial infections. | ||
== | ==Cytokines and cytokine signalling== | ||
In the course of screening, we find a lot of molecules and pathways that end up being involved in cytokine signalling and its consequences. One aspect of this is the metabolic effects of infection, which appear to result from high levels of cytokine expression over several days. Cytokines also regulate the realized immune response of the fly, much as they do in mammals. | |||
We've recently published some of this work in "Current Biology", showing that two different TGF-betas regulate fly immunity, each inhibiting a specific arm of the immune response, and each being produced by only a subset of phagocytes. [http://www.ncbi.nlm.nih.gov/pubmed/21962711 Check it out!] | |||
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Revision as of 12:27, 12 November 2011
Welcome to the Dionne lab!
That is to say, Marc Dionne's lab, at King's College London; not to be confused with any other Dionne lab.
We are interested in (1) the effects of host genetics on the biology of infection; and (2) cytokine signalling and its effects on immune and non-immune tissues. Drosophila melanogaster is our animal model of choice.
Work in the lab is funded by the Biotechnology and Biological Sciences Research Council and the Wellcome Trust.
We've moved!
The lab has moved from its original digs (on the 27th and 28th floors of Guy's Tower) across the street to New Hunt's House in order to be part of the new Centre for the Molecular and Cellular Biology of Inflammation. Our academic affiliation will be changing to the Peter Gorer Department of Immunobiology, DIIID, School of Medicine. Directions and postal addresses have been corrected on the Contact page.
Host genetics and the biology of infection
Different individuals show different levels of resistance to infections and develop different pathologies in response to infections. We are interested in why this is the case. We use the fruitfly Drosophila melanogaster as a model host to study these questions; this allows us to screen for genes that affect the progress of infection in a rapid and unbiased fashion.
All of our experiments originate from a simple genetic screen. Mutant flies are infected with Mycobacterium marinum, a bacterium closely-related to the causative agent of tuberculosis, or with Mycobacterium smegmatis, a related non-pathogen. We select lines of flies that die more quickly or more slowly than wild-type controls and identify the mutation that gives rise to this phenotype. We then try to understand what this phenotype tells us about the function of the mutated gene.
So far, our work on this system has focused on the mechanisms of pathogenesis. We have found that this infection causes progressive loss of metabolic stores, similar to the wasting seen in people with tuberculosis. We have shown that, in the fly, this wasting effect is caused partly by systemic failures in anabolic signals via the insulin effector kinase Akt. We are now working to try to understand how infection causes this defect in anabolic signalling. We also have mutants that affect other aspects of disease; we are working with these mutants to understand other aspects of disease pathogenesis as well as how the fly immune system fights Mycobacterial infections.
Cytokines and cytokine signalling
In the course of screening, we find a lot of molecules and pathways that end up being involved in cytokine signalling and its consequences. One aspect of this is the metabolic effects of infection, which appear to result from high levels of cytokine expression over several days. Cytokines also regulate the realized immune response of the fly, much as they do in mammals.
We've recently published some of this work in "Current Biology", showing that two different TGF-betas regulate fly immunity, each inhibiting a specific arm of the immune response, and each being produced by only a subset of phagocytes. Check it out!
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