Elucidation of molecular mechanism of immune evasion in malignant lymphoma

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K06840
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Tumor biology
• Research Institution: University of Tsukuba (2017); Keio University (2015-2016)
• Principal Investigator: Sugihara Eiji 筑波大学, 国際産学連携本部, 助教 (50464996)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 非ホジキンリンパ腫 / 腫瘍免疫 / Fas / Livin

Outline of Final Research Achievements

In this study, to examine how malignant lymphoma cells can escape from the immune system, our established mouse lymphoma model was analyzed. We found that Fas expression is downregulated in lymphoma cells, and that restoration of Fas expression by CD40 signal activation in lymphoma cells induces apoptosis triggered by cytotoxic T cells expressing Fas ligand. Furthermore, certain human lymphoma cell lines that highly express a member of Survivin family Livin show resistance to Fas-mediated apoptosis. Given that high expression of Livin is associated with poor prognosis in Non-Hodgkin's lymphoma patients, targeting Livin is a new therapeutic strategy for malignant lymphoma to restore anti-tumor immune activity by Fas-mediated apoptosis.

Free Research Field

腫瘍医学