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- Chang Chien-Chung
- Department of Immunology, Roswell Park Cancer Institute
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- Campoli Michael
- Department of Immunology, Roswell Park Cancer Institute
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- Ferrone Soldano
- Department of Immunology, Roswell Park Cancer Institute
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Depending on the tumor types, HLA class I antigen downregulation or loss has been found in 16% to 50% of malignant lesions in many malignancies with a clinical association with histopathological markers of poor prognosis of the disease and with reduced free interval and survival. These findings may reflect the escape of tumor cells with HLA class I abnormalities from recognition and destruction by HLA class I-restricted, tumor-associated antigen-specific cytotoxic T lymphocytes. This possibility has stimulated investigations on the mechanisms underlying HLA class I antigen abnormalities in malignant cells. Distinct molecular defects underlying an abnormal HLA class I phenotype have been identified and characterized. These defects range from structural alterations of the genes which encode HLA class I antigen subunits to deregulation of antigen processing machinery components responsible for a functional HLA class I antigen expression. These findings, in conjunction with those of clinical recurrence of lesions with HLA class I antigen loss following T cell-based immunotherapy in patients, suggests that immunoselection may play a role in the generation of malignant lesions with HLA class I antigen abnormalities. This possibility has stressed the need to effectively monitor functional HLA class I antigen expression in malignant lesions in the application of T cell-based immunotherapy as well as to develop strategies to circumvent the negative impact of immunoselection.
収録刊行物
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- The Keio Journal of Medicine
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The Keio Journal of Medicine 52 (4), 220-229, 2003
The Keio Journal of Medicine
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詳細情報 詳細情報について
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- CRID
- 1390282681314950528
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- NII論文ID
- 130000879621
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- NII書誌ID
- AA00710216
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- COI
- 1:CAS:528:DC%2BD2cXhvFOntLs%3D
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- ISSN
- 18801293
- 00229717
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- PubMed
- 14748474
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可