| Project/Area Number |
24500427
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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 |
Nerve anatomy/Neuropathology
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| Research Institution | Kurume University |
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Principal Investigator |
SUGITA YASUO 久留米大学, 医学部, 教授 (80216316)
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| Co-Investigator(Kenkyū-buntansha) |
OHSHIMA Koichi 久留米大学, 医学部, 教授 (50203766)
TERASAKI Mizuhiko 久留米大学, 医学部, 准教授 (70320223)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2014: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 中枢神経系原発悪性リンパ腫 / エンドセリンB受容体 / 免疫回避 / 腫瘍浸潤リンパ球 / ケモカイン / 腫瘍新生血管 / 免疫回避機構 / エンドセリン B 受容体 / 中枢神経原発悪性リンパ腫 / 中枢原発悪性リンパ腫 / 神経膠腫 |
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| Outline of Final Research Achievements |
In the present study, in order to clarify the immune escape mechanism of primary central nervous system lymphomas (PCNSL), the expression of endothelin B receptor (ETBR) and chemokines (CXCL12,13) in 24 PCNSL was investigated. CXCL12 was expressed by lymphoma cells in different brain cells in 22/24 cases. CXCL13 expression was identified in tumor cells in 18/24 cases. In addition, tumor infiltrated lymphocytes (TIL) accumulated in areas with expression of chemokines, particularly of CXCL13. ETBR expression was detected in 12/24 cases. Positive ETBR cases were associated with a paucity of TIL, particularly of cytotoxic T cells, whereas negative ETBR cases were associated with an abundance of TIL. These results indicate that CXCL12,13 up-regulation may be differently linked to the development of PCNSL and to the accumulation of TIL. In addition, ETBR expression by lymphoma and endothelial cells may mediate trafficking of TIL, which may explain the immune escape processes of PCNSL.
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