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dc.contributor.authorYano, Tamaki
dc.contributor.authorMita, Shizuka
dc.contributor.authorOhmori, Hiroko
dc.contributor.authorOshima, Yoshiteru
dc.contributor.authorFujimoto, Yukari
dc.contributor.authorUeda, Ryu
dc.contributor.authorTakada, Haruhiko
dc.contributor.authorGoldman, William E.
dc.contributor.authorFukase, Koichi
dc.contributor.authorSilverman, Neal S.
dc.contributor.authorYoshimori, Tamotsu
dc.contributor.authorKurata, Shoichiro
dc.date2022-08-11T08:09:09.000
dc.date.accessioned2022-08-23T16:19:10Z
dc.date.available2022-08-23T16:19:10Z
dc.date.issued2008-07-08
dc.date.submitted2009-12-15
dc.identifier.citationNat Immunol. 2008 Aug;9(8):908-16. Epub 2008 Jul 6. <a href="http://dx.doi.org/10.1038/ni.1634">Link to article on publisher's site</a>
dc.identifier.issn1529-2916 (Electronic)
dc.identifier.doi10.1038/ni.1634
dc.identifier.pmid18604211
dc.identifier.urihttp://hdl.handle.net/20.500.14038/34981
dc.description.abstractAutophagy, an evolutionally conserved homeostatic process for catabolizing cytoplasmic components, has been linked to the elimination of intracellular pathogens during mammalian innate immune responses. However, the mechanisms underlying cytoplasmic infection-induced autophagy and the function of autophagy in host survival after infection with intracellular pathogens remain unknown. Here we report that in drosophila, recognition of diaminopimelic acid-type peptidoglycan by the pattern-recognition receptor PGRP-LE was crucial for the induction of autophagy and that autophagy prevented the intracellular growth of Listeria monocytogenes and promoted host survival after this infection. Autophagy induction occurred independently of the Toll and IMD innate signaling pathways. Our findings define a pathway leading from the intracellular pattern-recognition receptors to the induction of autophagy to host defense.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=18604211&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1038/ni.1634
dc.subjectAnimals
dc.subject*Autophagy
dc.subjectDiaminopimelic Acid
dc.subjectDrosophila
dc.subjectImmunity, Innate
dc.subjectListeria
dc.subjectPeptidoglycan
dc.subjectToll-Like Receptors
dc.subjectImmunology and Infectious Disease
dc.titleAutophagic control of listeria through intracellular innate immune recognition in drosophila
dc.typeJournal Article
dc.source.journaltitleNature immunology
dc.source.volume9
dc.source.issue8
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/infdis_pp/20
dc.identifier.contextkey1088917
html.description.abstract<p>Autophagy, an evolutionally conserved homeostatic process for catabolizing cytoplasmic components, has been linked to the elimination of intracellular pathogens during mammalian innate immune responses. However, the mechanisms underlying cytoplasmic infection-induced autophagy and the function of autophagy in host survival after infection with intracellular pathogens remain unknown. Here we report that in drosophila, recognition of diaminopimelic acid-type peptidoglycan by the pattern-recognition receptor PGRP-LE was crucial for the induction of autophagy and that autophagy prevented the intracellular growth of Listeria monocytogenes and promoted host survival after this infection. Autophagy induction occurred independently of the Toll and IMD innate signaling pathways. Our findings define a pathway leading from the intracellular pattern-recognition receptors to the induction of autophagy to host defense.</p>
dc.identifier.submissionpathinfdis_pp/20
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages908-16


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