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Koda, Yuzo; Teratani, Toshiaki; Chu, Po-Sung; Hagihara, Yuya; Mikami, Yohei; Harada, Yosuke; Tsujikawa, Hanako; Miyamoto, Kentaro; Suzuki, Takahiro; Taniki, Nobuhito; Sujino, Tomohisa; Sakamoto, Michiie; Kanai, Takanori; Nakamoto, Nobuhiro
Nature communications, 07/2021, Letnik: 12, Številka: 1Journal Article
Abstract 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 + tissue-resident memory CD8 + T (CD8 + Trm) cells in resolving liver fibrosis. Single-cell transcriptome analysis and FACS analysis revealed CD69 + CD103 − CD8 + Trm cell enrichment in NASH resolution livers. The reduction of liver CD8 + Trm cells, maintained by tissue IL-15, significantly delayed fibrosis resolution, while adoptive transfer of these cells protected mice from fibrosis progression. During resolution, CD8 + Trm cells attracted hepatic stellate cells (HSCs) in a CCR5-dependent manner, and predisposed activated HSCs to FasL-Fas-mediated apoptosis. Histological assessment of patients with NASH revealed CD69 + CD8 + Trm abundance in fibrotic areas, further supporting their roles in humans. These results highlight the undefined role of liver CD8 + Trm in fibrosis resolution.
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