胃肠道B细胞可独立许可NASH微生物群中的代谢性T细胞活化，并通过IgA FcRy信号传导促成纤维化

Non-alcoholic steatohepatitis (NASH) is a T-cell mediated, auto-aggressive condition that can result in progressive liver disease and hepatocellular carcinoma. Gastrointestinal B-cells are activated and increased in number in mouse and human NASH, licensing metabolic-cell activation to induce NASH antigen- and microbiota-independently. Genetic or therapeutic depletion of B-cells systemically or gastrointestinal B-cells specifically prevented or reverted NASH and fibrosis. Clinical and molecular analyses from NASH patients demonstrated IgA-levels and activated FcRy+ hepatic myeloid cells to correlate with liver fibrosis degree.

非酒精性脂肪性肝炎（Non-alcoholic steatohepatitis, NASH）是一种T细胞介导的自身攻击性病症，可进展为进行性肝病并引发肝细胞癌。在小鼠与人类NASH患者体内，胃肠道B细胞被活化且数量增加，其可通过介导代谢细胞活化，在不依赖NASH抗原与肠道菌群的条件下诱导疾病发生。通过全身性或特异性靶向胃肠道B细胞的遗传或治疗性B细胞耗竭手段，能够阻止或逆转NASH及肝纤维化进程。针对NASH患者的临床与分子分析表明，免疫球蛋白A（IgA）水平与活化的FcRy阳性肝髓系细胞水平，均与肝纤维化程度呈显著相关。