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Article: Complementary activation of peripheral natural killer cell immunity in nasopharyngeal carcinoma

TitleComplementary activation of peripheral natural killer cell immunity in nasopharyngeal carcinoma
Authors
Issue Date2006
PublisherBlackwell Publishing Japan. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CAS
Citation
Cancer Science, 2006, v. 97 n. 9, p. 912-919 How to Cite?
AbstractNK cells and αβ- and γδ-CTL play important roles in cellular immunity against tumors. We previously demonstrated that NPC patients have a quantitative and qualitative deficit in γδ-CTL and EBV-specific αβ-CTL when compared to normal subjects and NPC long-term survivors. In this study we report further observations of a complementary activation of peripheral NK cells in NPC patients. The NK cells in these patients, compared to those of healthy subjects and NPC survivors, were preferentially activated in response to the stimulation of myeloma cell line XG-7 and expanded in the presence of exogenous IL-2. The production of IFN-γ was lowest in the patient group, whereas IL-12, IL-15 and TNF-α were produced in higher levels in patients than in the donors and survivors. The cytolytic effect of the NK cells against NPC cells in the patient group was also higher than that of the donors and survivors. Furthermore, the patients at later stages of NPC had lower γδ-CTL activity but higher NK cytotoxicity towards NPC targets, with higher production of IL-12, IL-15 and TNF-α but lower production of IFN-γ than in patients at earlier stages. This might be part of a triggered compensatory re-activation of the innate immunity, believed to be mediated through various cytokines and chemokines when adaptive T cell immunity is breached. Together, these data suggest complementary roles of innate and adaptive immune response in tumor immunity where NK cells, γδ- and αβ-CTL compensate for the deficits of one another at different stages of tumor invasion. © 2006 Japanese Cancer Association.
Persistent Identifierhttp://hdl.handle.net/10722/71891
ISSN
2015 Impact Factor: 3.896
2015 SCImago Journal Rankings: 1.744
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZheng, Yen_HK
dc.contributor.authorCao, KYen_HK
dc.contributor.authorNg, SPen_HK
dc.contributor.authorChua, DTTen_HK
dc.contributor.authorSham, JSTen_HK
dc.contributor.authorKwong, DLWen_HK
dc.contributor.authorNg, MHen_HK
dc.contributor.authorLu, Len_HK
dc.contributor.authorZheng, BJen_HK
dc.date.accessioned2010-09-06T06:36:11Z-
dc.date.available2010-09-06T06:36:11Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Science, 2006, v. 97 n. 9, p. 912-919en_HK
dc.identifier.issn1347-9032en_HK
dc.identifier.urihttp://hdl.handle.net/10722/71891-
dc.description.abstractNK cells and αβ- and γδ-CTL play important roles in cellular immunity against tumors. We previously demonstrated that NPC patients have a quantitative and qualitative deficit in γδ-CTL and EBV-specific αβ-CTL when compared to normal subjects and NPC long-term survivors. In this study we report further observations of a complementary activation of peripheral NK cells in NPC patients. The NK cells in these patients, compared to those of healthy subjects and NPC survivors, were preferentially activated in response to the stimulation of myeloma cell line XG-7 and expanded in the presence of exogenous IL-2. The production of IFN-γ was lowest in the patient group, whereas IL-12, IL-15 and TNF-α were produced in higher levels in patients than in the donors and survivors. The cytolytic effect of the NK cells against NPC cells in the patient group was also higher than that of the donors and survivors. Furthermore, the patients at later stages of NPC had lower γδ-CTL activity but higher NK cytotoxicity towards NPC targets, with higher production of IL-12, IL-15 and TNF-α but lower production of IFN-γ than in patients at earlier stages. This might be part of a triggered compensatory re-activation of the innate immunity, believed to be mediated through various cytokines and chemokines when adaptive T cell immunity is breached. Together, these data suggest complementary roles of innate and adaptive immune response in tumor immunity where NK cells, γδ- and αβ-CTL compensate for the deficits of one another at different stages of tumor invasion. © 2006 Japanese Cancer Association.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Japan. The Journal's web site is located at http://www.blackwellpublishing.com/journals/CASen_HK
dc.relation.ispartofCancer Scienceen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAsian Continental Ancestry Groupen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCytokines - biosynthesisen_HK
dc.subject.meshCytotoxicity, Immunologicen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshHumansen_HK
dc.subject.meshKiller Cells, Natural - immunologyen_HK
dc.subject.meshLymphocyte Activation - immunologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNasopharyngeal Neoplasms - immunology - mortalityen_HK
dc.subject.meshT-Lymphocytes, Cytotoxic - immunologyen_HK
dc.titleComplementary activation of peripheral natural killer cell immunity in nasopharyngeal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1347-9032&volume=97&issue=9&spage=912&epage=9&date=2006&atitle=Complementary+activation+of+peripheral+natural+killer+cell+immunity+in+nasopharyngeal+carcinomaen_HK
dc.identifier.emailChua, DTT: dttchua@hkucc.hku.hken_HK
dc.identifier.emailKwong, DLW: dlwkwong@hku.hken_HK
dc.identifier.emailLu, L: liweilu@hkucc.hku.hken_HK
dc.identifier.emailZheng, BJ: bzheng@hkucc.hku.hken_HK
dc.identifier.authorityChua, DTT=rp00415en_HK
dc.identifier.authorityKwong, DLW=rp00414en_HK
dc.identifier.authorityLu, L=rp00477en_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1111/j.1349-7006.2006.00252.xen_HK
dc.identifier.pmid16805822-
dc.identifier.scopuseid_2-s2.0-33746657236en_HK
dc.identifier.hkuros120559en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33746657236&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume97en_HK
dc.identifier.issue9en_HK
dc.identifier.spage912en_HK
dc.identifier.epage919en_HK
dc.identifier.isiWOS:000239454000017-
dc.publisher.placeJapanen_HK
dc.identifier.scopusauthoridZheng, Y=7404838014en_HK
dc.identifier.scopusauthoridCao, KY=15845100900en_HK
dc.identifier.scopusauthoridNg, SP=8862966400en_HK
dc.identifier.scopusauthoridChua, DTT=7006773480en_HK
dc.identifier.scopusauthoridSham, JST=7101655565en_HK
dc.identifier.scopusauthoridKwong, DLW=15744231600en_HK
dc.identifier.scopusauthoridNg, MH=7202076421en_HK
dc.identifier.scopusauthoridLu, L=7403963552en_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.citeulike783943-

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