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dc.contributor.authorBoyer, Laurent
dc.contributor.authorMagoc, Lorin
dc.contributor.authorDejardin, Stephanie
dc.contributor.authorCappillino, Michael
dc.contributor.authorPaquette, Nicholas Paul
dc.contributor.authorHinault, Charlotte
dc.contributor.authorCharriere, Guillaume M.
dc.contributor.authorIp, W. K. Eddie
dc.contributor.authorFracchia, Shannon
dc.contributor.authorHennessy, Elizabeth
dc.contributor.authorErturk Hasdemir, Deniz
dc.contributor.authorReichhart, Jean-Marc
dc.contributor.authorSilverman, Neal S.
dc.contributor.authorLucy-Hulbert, Adam
dc.contributor.authorStuart, Lynda M.
dc.date2022-08-11T08:09:08.000
dc.date.accessioned2022-08-23T16:18:57Z
dc.date.available2022-08-23T16:18:57Z
dc.date.issued2011-10-28
dc.date.submitted2013-01-31
dc.identifier.citationImmunity. 2011 Oct 28;35(4):536-49. doi: 10.1016/j.immuni.2011.08.015. <a href="http://dx.doi.org/10.1016/j.immuni.2011.08.015" target="_blank">Link to article on publisher's site</a>
dc.identifier.issn1074-7613 (Linking)
dc.identifier.doi10.1016/j.immuni.2011.08.015
dc.identifier.pmid22018470
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34931
dc.description.abstractAlthough infections with virulent pathogens often induce a strong inflammatory reaction, what drives the increased immune response to pathogens compared to nonpathogenic microbes is poorly understood. One possibility is that the immune system senses the level of threat from a microorganism and augments the response accordingly. Here, focusing on cytotoxic necrotizing factor 1 (CNF1), an Escherichia coli-derived effector molecule, we showed the host indirectly sensed the pathogen by monitoring for the effector that modified RhoGTPases. CNF1 modified Rac2, which then interacted with the innate immune adaptors IMD and Rip1-Rip2 in flies and mammalian cells, respectively, to drive an immune response. This response was protective and increased the ability of the host to restrict pathogen growth, thus defining a mechanism of effector-triggered immunity that contributes to how metazoans defend against microbes with pathogenic potential.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=22018470&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258503/pdf/nihms331006.pdf
dc.subjectAdaptor Proteins, Signal Transducing
dc.subjectEnzyme Activation
dc.subjectHEK293 Cells
dc.subjectHumans
dc.subjectReceptor-Interacting Protein Serine-Threonine Kinases
dc.subject*Signal Transduction
dc.subjectrac GTP-Binding Proteins
dc.subjectImmunology and Infectious Disease
dc.titlePathogen-derived effectors trigger protective immunity via activation of the Rac2 enzyme and the IMD or Rip kinase signaling pathway
dc.typeJournal Article
dc.source.journaltitleImmunity
dc.source.volume35
dc.source.issue4
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/infdis_pp/155
dc.identifier.contextkey3631098
html.description.abstract<p>Although infections with virulent pathogens often induce a strong inflammatory reaction, what drives the increased immune response to pathogens compared to nonpathogenic microbes is poorly understood. One possibility is that the immune system senses the level of threat from a microorganism and augments the response accordingly. Here, focusing on cytotoxic necrotizing factor 1 (CNF1), an Escherichia coli-derived effector molecule, we showed the host indirectly sensed the pathogen by monitoring for the effector that modified RhoGTPases. CNF1 modified Rac2, which then interacted with the innate immune adaptors IMD and Rip1-Rip2 in flies and mammalian cells, respectively, to drive an immune response. This response was protective and increased the ability of the host to restrict pathogen growth, thus defining a mechanism of effector-triggered immunity that contributes to how metazoans defend against microbes with pathogenic potential.</p>
dc.identifier.submissionpathinfdis_pp/155
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages536-49


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