Interleukin-27 dependent loss of memory CD4+ T-cells after malaria infection

2022 Fiscal Year Final Research Report

• Project/Area Number: 19K07528
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 49040:Parasitology-related
• Research Institution: Kobe Women's University
• Principal Investigator: Kimura Daisuke 神戸女子大学, 健康福祉学部, 教授 (50423637)
• Co-Investigator(Kenkyū-buntansha): 由井 克之 長崎大学, 医歯薬学総合研究科(医学系), 教授 (90274638)
• Project Period (FY): 2019-04-01 – 2023-03-31
• Keywords: マラリア / 免疫記憶 / CD4陽性T細胞 / アポトーシス / 溶血性貧血

Outline of Final Research Achievements

The reason why malaria is difficult to control is that Plasmodium falciparum infection does not maintain immune memory. Previously, we have shown that in a mouse model of malaria infection, activated CD4+ T cells die early after infection, but not in IL-27 receptor-deficient mice. Interestingly, this phenomenon was also observed in mice with drug-induced hemolytic anemia. This suggests that erythrocyte components destroyed by the malaria parasite prevent long-term survival of malaria-specific CD4+ T cells. The relationship between erythrocyte components and IL-27 signaling is currently being analyzed.

Free Research Field

感染免疫

Academic Significance and Societal Importance of the Research Achievements

本研究目的である「IL-27による免疫記憶抑制メカニズム解明」は、これまでの我々独自の研究成果を発展させたものである。また、記憶T細胞の細胞死を誘発させる赤血球成分を特定できれば、記憶抑制メカニズムが明らかとなり、将来完成が期待されるワクチン効果を促進・維持させることで、マラリアワクチン開発へ向けて貢献ができる。また、これまで研究されてきた既存のワクチン候補中に本研究成果と組み合わせることで、効果が期待できる可能性も考えられる。