Development of a new therapeutic strategy regulated Treg cells targeting protein tyrosine phosphatase non-receptor type 3 (PTPN3)

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K09047
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 55010:General surgery and pediatric surgery-related
• Research Institution: Kyushu University
• Principal Investigator: NAGAMI Masayo (梅林雅代) 九州大学, 医学研究院, 共同研究員 (80792209)
• Co-Investigator(Kenkyū-buntansha): 大西 秀哉 九州大学, 医学研究院, 准教授 (30553276) ; 三好 圭 九州大学, 大学病院, 助教 (70755272) ; 森崎 隆 九州大学, 医学研究院, 共同研究員 (90291517) ; 永井 俊太郎 九州大学, 大学病院, 助教 (90755240)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 制御性T細胞 / PTPN3 / CD8T細胞 / 細胞性免疫能亢進 / 癌組織線維化 / 癌微小環境 / 癌浸潤リンパ球 / 免疫寛容

Outline of Final Research Achievements

FOXP3+Treg cells and CD8+T cells numbers were compared with PTPN3 high expression area and PTPN3 low expression area in resected small cell lung cancer specimen. In PTPN3 high expression area cancer fibrosis is high, infiltrated FOXP3+Treg number is high and infiltrated CD8+T cell number is low. On the contrary, in PTPN3 low expression area cancer fibrosis is low, infiltrated FOXP3+Treg number is low and infiltrated CD8+T cell number is high. These results suggest that PTPN3 expression in cancer tissue contribute to the decrease of cancer tissue-infiltrated CD8/Treg cell number ratio and that it induces immune tolerance.

Free Research Field

腫瘍免疫学

Academic Significance and Societal Importance of the Research Achievements

PTPN3分子が小細胞肺癌において、FOXP3+Treg細胞の浸潤増加、CD8+T細胞の浸潤低下を制御していることが示唆され、PTPN3抑制が細胞性免疫能亢進を惹起するすることが示唆された。その機序として癌線維化の関与が示唆され、PTPN3抑制が癌微小環境の制御にも作用すること可能性が考えられた。