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
✍ Scribed by Lijun Shen; Alan K.S. Chiang; Wei Ping Liu; Gan Di Li; Raymond H.S. Liang; Gopesh Srivastava
- Publisher
- John Wiley and Sons
- Year
- 2001
- Tongue
- French
- Weight
- 536 KB
- Volume
- 92
- Category
- Article
- ISSN
- 0020-7136
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✦ Synopsis
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  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,  2 -microglobulin and TAP1 on most tumor cells, except for two cases (5%) in which most of the tumor cells lacked  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.