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Article: Expression of HLA class I, β2-microglobulin, TAP1 and IL-10 in epstein-barr virus-associated nasal NK/T-cell lymphoma: Implications for tumor immune escape mechanism

TitleExpression of HLA class I, β2-microglobulin, TAP1 and IL-10 in epstein-barr virus-associated nasal NK/T-cell lymphoma: Implications for tumor immune escape mechanism
Authors
Keywordsβ2-microglobulin
Epstein-Barr virus
HLA class 1,immune escape
Interleukin-10
Nasal NK/T-cell lymphoma
TAP 1
Issue Date2001
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2001, v. 92 n. 5, p. 692-696 How to Cite?
AbstractSeveral mechanisms of immune escape might be in operation in Epstein-Barr virus (EBV)-associated nasal NK/T-cell lymphoma. We have previously shown the downregulation of the immunogenic EBV nuclear antigens by alternative promoter usage and the preferential selection of the deletion genotype of latent membrane protein I in nasal lymphoma. To understand further the strategies used for immune escape by this tumor, we examined by immunohistochemistry HLA class I expression in 15 cases using frozen sections, along with β2-microglobulin and transporter associated with antigen processing I (TAPI) expression in 39 cases using paraffin sections. All nasal NK/T-cell lymphomas showed positive staining for HLA class I, β2-microglobulin and TAP I on most tumor cells, except for two cases (5%) in which most of the tumor cells lacked β2-microglobulin staining. We next immunostained for interleukin-10 on frozen sections in 13 cases, all of which showed strong expression by most tumor cells. Transcription of human interleukin-10 but not EBV BCRF I (viral interleukin-10) was identified by reverse transcriptase-polymerase chain reaction in these nasal NK/T-cell lymphomas. Overall, our data suggest that global downregulation of HLA class I or TAP I rarely accounts for the ability of nasal NK/T-cell lymphoma to evade immunosurveillance and that other immune escape mechanisms may be operating in nasal NK/T-cell lymphoma, such as production of interleukin-10 to suppress the local immune response. © 2001 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/148251
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShen, Len_HK
dc.contributor.authorChiang, AKSen_HK
dc.contributor.authorLiu, WPen_HK
dc.contributor.authorLi, GDen_HK
dc.contributor.authorLiang, RHSen_HK
dc.contributor.authorSrivastava, Gen_HK
dc.date.accessioned2012-05-29T06:11:48Z-
dc.date.available2012-05-29T06:11:48Z-
dc.date.issued2001en_HK
dc.identifier.citationInternational Journal Of Cancer, 2001, v. 92 n. 5, p. 692-696en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148251-
dc.description.abstractSeveral mechanisms of immune escape might be in operation in Epstein-Barr virus (EBV)-associated nasal NK/T-cell lymphoma. We have previously shown the downregulation of the immunogenic EBV nuclear antigens by alternative promoter usage and the preferential selection of the deletion genotype of latent membrane protein I in nasal lymphoma. To understand further the strategies used for immune escape by this tumor, we examined by immunohistochemistry HLA class I expression in 15 cases using frozen sections, along with β2-microglobulin and transporter associated with antigen processing I (TAPI) expression in 39 cases using paraffin sections. All nasal NK/T-cell lymphomas showed positive staining for HLA class I, β2-microglobulin and TAP I on most tumor cells, except for two cases (5%) in which most of the tumor cells lacked β2-microglobulin staining. We next immunostained for interleukin-10 on frozen sections in 13 cases, all of which showed strong expression by most tumor cells. Transcription of human interleukin-10 but not EBV BCRF I (viral interleukin-10) was identified by reverse transcriptase-polymerase chain reaction in these nasal NK/T-cell lymphomas. Overall, our data suggest that global downregulation of HLA class I or TAP I rarely accounts for the ability of nasal NK/T-cell lymphoma to evade immunosurveillance and that other immune escape mechanisms may be operating in nasal NK/T-cell lymphoma, such as production of interleukin-10 to suppress the local immune response. © 2001 Wiley-Liss, Inc.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.-
dc.subjectβ2-microglobulinen_HK
dc.subjectEpstein-Barr virusen_HK
dc.subjectHLA class 1,immune escapeen_HK
dc.subjectInterleukin-10en_HK
dc.subjectNasal NK/T-cell lymphomaen_HK
dc.subjectTAP 1en_HK
dc.subject.meshAtp-Binding Cassette Transporters - Analysisen_US
dc.subject.meshEpstein-Barr Virus Infections - Immunologyen_US
dc.subject.meshHistocompatibility Antigens Class I - Analysisen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshInterleukin-10 - Analysisen_US
dc.subject.meshLymphoma, T-Cell - Immunologyen_US
dc.subject.meshNose Neoplasms - Immunologyen_US
dc.subject.meshBeta 2-Microglobulin - Analysisen_US
dc.titleExpression of HLA class I, β2-microglobulin, TAP1 and IL-10 in epstein-barr virus-associated nasal NK/T-cell lymphoma: Implications for tumor immune escape mechanismen_HK
dc.typeArticleen_HK
dc.identifier.emailChiang, AKS:chiangak@hkucc.hku.hken_HK
dc.identifier.emailLiang, RHS:rliang@hku.hken_HK
dc.identifier.emailSrivastava, G:gopesh@pathology.hku.hken_HK
dc.identifier.authorityChiang, AKS=rp00403en_HK
dc.identifier.authorityLiang, RHS=rp00345en_HK
dc.identifier.authoritySrivastava, G=rp00365en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/1097-0215(20010601)92:5<692::AID-IJC1237>3.0.CO;2-Zen_HK
dc.identifier.pmid11340574-
dc.identifier.scopuseid_2-s2.0-0035371668en_HK
dc.identifier.hkuros56983-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035371668&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume92en_HK
dc.identifier.issue5en_HK
dc.identifier.spage692en_HK
dc.identifier.epage696en_HK
dc.identifier.isiWOS:000168420400013-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShen, L=7401704659en_HK
dc.identifier.scopusauthoridChiang, AKS=7101623534en_HK
dc.identifier.scopusauthoridLiu, WP=24312055100en_HK
dc.identifier.scopusauthoridLi, GD=8379895000en_HK
dc.identifier.scopusauthoridLiang, RHS=26643224900en_HK
dc.identifier.scopusauthoridSrivastava, G=7202242238en_HK

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