Loss of tapasin limits HLA class I antigen processing and results in escape from CTL responses to cancer cells
| Project/Area Number |
26460581
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 腫瘍免疫 / 免疫逃避 / 抗原提示 / HLAクラスI / tapasin / CTL / Tapasin / がん免疫療法 |
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| Outline of Final Research Achievements |
Understanding the mechanisms by which cancers escape from immune surveillance is an issue of wide importance. In this study, we show that tapasin expression is decreased in more than 70% of the cancer tissues of non-small cell lung cancer patients, and positively correlated with patient survivals. The further experiments using tapasin-deficient cancer models demonstrate that loss of tapasin expression leads to escape from tumor-associated antigen (TAA) specific T-cell recognition. Tapasin-deficient cancer cells produce reduced amounts of TAAs and are resistant to cytotoxic T-cell responses both in vitro and in vivo. Thus, tapasin expression is a key for T-cell mediated immune surveillance against human cancers.
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Report
(4 results)
Research Products
(11 results)
