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Article: A role for double-stranded RNA-activated protein kinase PKR in Mycobacterium-induced cytokine expression

TitleA role for double-stranded RNA-activated protein kinase PKR in Mycobacterium-induced cytokine expression
Authors
Issue Date2005
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
Journal Of Immunology, 2005, v. 175 n. 11, p. 7218-7225 How to Cite?
AbstractFollowing infection of the host by Mycobacterium tuberculosis, induction of cytokines is a major defense mechanism to limit the pathogen invasion. Cytokines interact with each other to form an intertwined network of pathways. For example, IFN and TNF have been shown to interact through common pathways including IFN-inducible, dsRNA-activated serine/threonine protein kinase (PKR) induction. As a signal transducer, it has been conventionally known to regulate the induction of cytokine expression in response to virus infection through NF-κB. In light of the critical role of TNF in immunity and its cytotoxic effects mediated by PKR, we examined the role of the kinase in the regulation of immune response against M. tuberculosis using the interaction of bacillus Calmette-Guérin (BCG) and primary human blood monocytes as a model. Our results showed that BCG stimulates the induction of cytokine expression in human primary blood monocytes including TNF-α, IL-6, and IL-10. With the suppression of PKR by using PKR-mutant gene or 2-aminopurine as PKR inhibitor, we showed that the BCG-induced cytokine expression in human monocytes is regulated by the phosphorylation and activation of PKR. We also demonstrated that downstream of PKR induction is the activation of MAPK and translocation of NF-κB into the nucleus. NF-κB in turn mediates the transcription of specific cytokine genes. Taken together, PKR plays a critical role in the regulation of immune responses to mycobacterial infection and may serve as an important molecule in the innate antimycobacterial defense. Copyright © 2005 by The American Association of Immunologists, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/49263
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, BKWen_HK
dc.contributor.authorLee, DCWen_HK
dc.contributor.authorLi, JCBen_HK
dc.contributor.authorLau, YLen_HK
dc.contributor.authorLau, ASYen_HK
dc.date.accessioned2008-06-12T06:37:57Z-
dc.date.available2008-06-12T06:37:57Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Immunology, 2005, v. 175 n. 11, p. 7218-7225en_HK
dc.identifier.issn0022-1767en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49263-
dc.description.abstractFollowing infection of the host by Mycobacterium tuberculosis, induction of cytokines is a major defense mechanism to limit the pathogen invasion. Cytokines interact with each other to form an intertwined network of pathways. For example, IFN and TNF have been shown to interact through common pathways including IFN-inducible, dsRNA-activated serine/threonine protein kinase (PKR) induction. As a signal transducer, it has been conventionally known to regulate the induction of cytokine expression in response to virus infection through NF-κB. In light of the critical role of TNF in immunity and its cytotoxic effects mediated by PKR, we examined the role of the kinase in the regulation of immune response against M. tuberculosis using the interaction of bacillus Calmette-Guérin (BCG) and primary human blood monocytes as a model. Our results showed that BCG stimulates the induction of cytokine expression in human primary blood monocytes including TNF-α, IL-6, and IL-10. With the suppression of PKR by using PKR-mutant gene or 2-aminopurine as PKR inhibitor, we showed that the BCG-induced cytokine expression in human monocytes is regulated by the phosphorylation and activation of PKR. We also demonstrated that downstream of PKR induction is the activation of MAPK and translocation of NF-κB into the nucleus. NF-κB in turn mediates the transcription of specific cytokine genes. Taken together, PKR plays a critical role in the regulation of immune responses to mycobacterial infection and may serve as an important molecule in the innate antimycobacterial defense. Copyright © 2005 by The American Association of Immunologists, Inc.en_HK
dc.format.extent420 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.orgen_HK
dc.relation.ispartofJournal of Immunologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThis is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (The AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). The AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.orgen_HK
dc.subject.meshCytokines - biosynthesisen_HK
dc.subject.meshMonocytes - immunology - microbiologyen_HK
dc.subject.meshMycobacterium Infections - immunologyen_HK
dc.subject.mesheIF-2 Kinase - immunology - metabolismen_HK
dc.subject.meshU937 Cellsen_HK
dc.titleA role for double-stranded RNA-activated protein kinase PKR in Mycobacterium-induced cytokine expressionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1767&volume=175&issue=11&spage=7218&epage=7225&date=2005&atitle=A+role+for+double-stranded+RNA-activated+protein+kinase+PKR+in+Mycobacterium-induced+cytokine+expressionen_HK
dc.identifier.emailLi, JCB: jamesli@hku.hken_HK
dc.identifier.emailLau, YL: lauylung@hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.authorityLi, JCB=rp00496en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid16301626-
dc.identifier.scopuseid_2-s2.0-28244437069en_HK
dc.identifier.hkuros114301-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-28244437069&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume175en_HK
dc.identifier.issue11en_HK
dc.identifier.spage7218en_HK
dc.identifier.epage7225en_HK
dc.identifier.isiWOS:000233544200020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, BKW=9634391200en_HK
dc.identifier.scopusauthoridLee, DCW=15751156000en_HK
dc.identifier.scopusauthoridLi, JCB=23103447500en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.scopusauthoridLau, ASY=7202626202en_HK

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