Mori Taizo, Yoshio Sachiyo, Kakazu Eiji, Kanto Tatsuya
Department of Liver Diseases, The Research Center for Hepatitis and Immunology, National Center for Global Health and Medicine, Chiba, Japan.
Gastroenterol Rep (Oxf). 2024 Oct 15;12:goae089. doi: 10.1093/gastro/goae089. eCollection 2024.
Non-alcoholic fatty liver disease, recently renamed metabolic dysfunction-associated steatotic liver disease (MASLD), is a complex multifactorial disease that progresses from steatohepatitis (MASH) to liver cirrhosis and liver cancer. Recent research has revealed that crosstalk between innate immune cells and hepatic parenchymal and non-parenchymal cells is involved in the pathogenesis of liver disease in MASLD/MASH. Of particular importance, novel inflammatory mechanisms, including macrophage diversity, neutrophil NETosis, B-cell biology, auto-reactive T cells, unconventional T cells, and dendritic cell-T cell interactions, are considered key drivers for disease progression. These mechanisms and factors are potential targets for the therapeutic intervention of MASLD/MASH. In this review, we focus on recent discoveries related to liver inflammation and discuss the role of innate immune cell subsets in MASLD/MASH.
非酒精性脂肪性肝病，最近更名为代谢功能障碍相关脂肪性肝病（MASLD），是一种复杂的多因素疾病，可从脂肪性肝炎（MASH）发展为肝硬化和肝癌。最近的研究表明，先天性免疫细胞与肝实质细胞和非实质细胞之间的相互作用参与了MASLD/MASH中肝脏疾病的发病机制。特别重要的是，包括巨噬细胞多样性、中性粒细胞胞外陷阱形成、B细胞生物学、自身反应性T细胞、非常规T细胞以及树突状细胞与T细胞相互作用在内的新型炎症机制被认为是疾病进展的关键驱动因素。这些机制和因素是MASLD/MASH治疗干预的潜在靶点。在本综述中，我们重点关注与肝脏炎症相关的最新发现，并讨论先天性免疫细胞亚群在MASLD/MASH中的作用。
