慶應義塾大学 · Medicine
칸아이 타카노리 교수의 연구실은 간질환, 특히 비알코올성간지방성염증성간경변(NASH)의 회복 메커니즘과 장내 미생물, 면역세포의 역할을 중심으로 연구를 진행하고 있습니다. 특히 CD8+ 조직기억 T세포와 장내 세균인 *F. saccharivorans* 가 간 섬유화 회복 및 염증 조절에 기여하는 메커니즘을 규명하고 있으며, 면역 체크포인트 분자인 PD-1 및 그 리간드의 면역 조절 기능을 탐색하고 있습니다. 이는 만성 염증성 질환의 새로운 치료 전략 개발에 기여할 잠재력을 지닙니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Non-alcoholic steatohepatitis (NASH) is a leading cause of chronic liver disease that can progress to liver fibrosis. Recent clinical advance suggests a reversibility of liver fibrosis, but the cellular and molecular mechanisms underlying NASH resolution remain unclarified. Here, using a murine diet-induced NASH and the subsequent resolution model, we demonstrate direct roles of CD8<sup>+</sup> tissue-resident memory CD8<sup>+</sup> T (CD8<sup>+</sup> Trm) cells in resolving liver fibrosis. Sing
F. saccharivorans decreased in correlation to UC activity and suppresses intestinal inflammation. These results suggest that F. saccharivorans could lead to a novel UC treatment.
A newly identified costimulatory molecule, programmed death-1 (PD-1), provides a negative signal that is essential for immune homeostasis. However, it has been suggested that its ligands, B7-H1 (PD-L1) and B7-dendritic cells (B7-DC; PD-L2), could also costimulate T cell proliferation and cytokine secretion. Here we demonstrate the involvement of PD-1/B7-H1 and B7-DC interaction in the development of colitis. We first examined the expression profiles of PD-1 and its ligands in both human inflamma
