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dc.contributor.authorVladimer, Gregory I.
dc.contributor.authorWeng, Dan
dc.contributor.authorPaquette, Sara W. Montminy
dc.contributor.authorVanaja, Sivapriya Kailasan
dc.contributor.authorRathinam, Vijay A.K.
dc.contributor.authorAune, Marie Hjelmseth
dc.contributor.authorConlon, Joseph E.
dc.contributor.authorBurbage, Joseph J.
dc.contributor.authorProulx, Megan K.
dc.contributor.authorLiu, Qin
dc.contributor.authorReed, George W.
dc.contributor.authorMecsas, Joan C.
dc.contributor.authorIwakura, Yoichiro
dc.contributor.authorBertin, John
dc.contributor.authorGoguen, Jon D.
dc.contributor.authorFitzgerald, Katherine A.
dc.contributor.authorLien, Egil
dc.date2022-08-11T08:08:54.000
dc.date.accessioned2022-08-23T16:11:46Z
dc.date.available2022-08-23T16:11:46Z
dc.date.issued2012-07-27
dc.date.submitted2012-07-31
dc.identifier.citation<p>Immunity. 2012 Jul 27;37(1):96-107. DOI 10.1016/j.immuni.2012.07.006</p>
dc.identifier.issn1097-4180
dc.identifier.doi10.1016/j.immuni.2012.07.006
dc.identifier.pmid22840842
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33248
dc.description.abstractYersinia pestis, the causative agent of plague, is able to suppress production of inflammatory cytokines IL-18 and IL-1β, which are generated through caspase-1-activating nucleotide-binding domain and leucine-rich repeat (NLR)-containing inflammasomes. Here, we sought to elucidate the role of NLRs and IL-18 during plague. Lack of IL-18 signaling led to increased susceptibility to Y. pestis, producing tetra-acylated lipid A, and an attenuated strain producing a Y. pseudotuberculosis-like hexa-acylated lipid A. We found that the NLRP12 inflammasome was an important regulator controlling IL-18 and IL-1β production after Y. pestis infection, and NLRP12-deficient mice were more susceptible to bacterial challenge. NLRP12 also directed interferon-γ production via induction of IL-18, but had minimal effect on signaling to the transcription factor NF-κB. These studies reveal a role for NLRP12 in host resistance against pathogens. Minimizing NLRP12 inflammasome activation may have been a central factor in evolution of the high virulence of Y. pestis.
dc.language.isoen_US
dc.publisherCell Press
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=22840842&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.immuni.2012.07.006
dc.subjectImmunity, Innate; Inflammasomes; Intracellular Signaling Peptides and Proteins; Interleukin-18; Interleukin-1beta; Yersinia pestis
dc.subjectimmunology
dc.subjectinfectious disease
dc.subjectinnate immunology
dc.subjectImmunity
dc.subjectImmunology of Infectious Disease
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.subjectPathogenic Microbiology
dc.titleThe NLRP12 Inflammasome Recognizes Yersinia pestis
dc.typeJournal Article
dc.source.journaltitleImmunity
dc.source.volume37
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2792&amp;context=gsbs_sp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1782
dc.identifier.contextkey3161834
refterms.dateFOA2022-08-23T16:11:46Z
html.description.abstract<p><em>Yersinia pestis</em>, the causative agent of plague, is able to suppress production of inflammatory cytokines IL-18 and IL-1β, which are generated through caspase-1-activating nucleotide-binding domain and leucine-rich repeat (NLR)-containing inflammasomes. Here, we sought to elucidate the role of NLRs and IL-18 during plague. Lack of IL-18 signaling led to increased susceptibility to <em>Y. pestis</em>, producing tetra-acylated lipid A, and an attenuated strain producing a Y. pseudotuberculosis-like hexa-acylated lipid A. We found that the NLRP12 inflammasome was an important regulator controlling IL-18 and IL-1β production after<em> Y. pestis</em> infection, and NLRP12-deficient mice were more susceptible to bacterial challenge. NLRP12 also directed interferon-γ production via induction of IL-18, but had minimal effect on signaling to the transcription factor NF-κB. These studies reveal a role for NLRP12 in host resistance against pathogens. Minimizing NLRP12 inflammasome activation may have been a central factor in evolution of the high virulence of <em>Y. pestis</em>.</p>
dc.identifier.submissionpathgsbs_sp/1782
dc.contributor.departmentDepartment of Medicine, Division of Preventive and Behavioral Medicine
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.contributor.departmentDepartment of Medicine, Division of Infectious Disease and Immunology
dc.source.pages96-107
dc.contributor.studentGregory I. Vladimer; Dan Weng


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