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Expression of HLA class I, β 2 ‐microglobulin, TAP1 and IL‐10 in Epstein‐Barr virus‐associated nasal NK/T‐cell lymphoma: Implications for tumor immune escape mechanism
Author(s) -
Shen Lijun,
Chiang Alan K.S.,
Liu Wei Ping,
Li Gan Di,
Liang Raymond H.S.,
Srivastava Gopesh
Publication year - 2001
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(20010601)92:5<692::aid-ijc1237>3.0.co;2-z
Subject(s) - mhc class i , biology , human leukocyte antigen , lymphoma , immune system , immunology , major histocompatibility complex , cancer research , beta 2 microglobulin , immunosurveillance , antigen , epstein–barr virus , virus
Several 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 1 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 β 2 ‐microglobulin and transporter associated with antigen processing 1 (TAP1) expression in 39 cases using paraffin sections. All nasal NK/T‐cell lymphomas showed positive staining for HLA class I, β 2 ‐microglobulin and TAP1 on most tumor cells, except for two cases (5%) in which most of the tumor cells lacked β 2 ‐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 BCRF1 (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 TAP1 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.