Analysis of tumor immunity in autoimmune conditions promoting tumorigenesis

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K18484
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57020:Oral pathobiological science-related
• Research Institution: The University of Tokushima (2022); Kagoshima University (2020-2021)
• Principal Investigator: KONDO Tomoyuki 徳島大学, 大学院医歯薬学研究部(医学域), 助教 (10782873)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 腫瘍免疫 / 自己免疫疾患 / 化学発がん

Outline of Final Research Achievements

In an autoimmune disease model (B6/lpr mice), chemical carcinogenesis induced the development of qualitatively more malignant tumors and increased tumor growth compared to controls (C57/BL6 mice).The expression of the inhibitory immune checkpoint molecule PD-1 was increased in both peripheral blood and tumor tissue of B6/lpr mice.Furthermore, T cells from B6/lpr mice readily expressed PD-1 by activation-stimulus compared to controls.
These findings suggest that T cell PD-1 expression is readily enhanced in autoimmune conditions, which may promote tumorigenesis due to impaired tumor immunity.

Free Research Field

免疫学

Academic Significance and Societal Importance of the Research Achievements

自己免疫疾患患者では腫瘍発生リスクが亢進するという報告はあるものの、自己免疫状態の腫瘍発生への関与は不明な点が多い。本研究では腫瘍発生自己免疫疾患モデルマウスの解析によって、自己免疫状態では免疫チェックポイント分子PD-1の発現がT細胞で容易に惹起される事によって腫瘍免疫が抑制され、腫瘍発生が亢進することを見出した。この結果は複雑な腫瘍免疫システムの制御への一助となる可能性がある。