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肝脏不仅具备造血、代谢和解毒等多重功能，还凭借其独特的免疫耐受微环境成为人体重要的免疫器官，可通过调节抗病毒免疫应答、凝血和抗凝血系统平衡影响乙型肝炎重症化/肝衰竭的疾病进展和临床预后。
1.作为识别乙型肝炎病毒及其产物的第一感受器，模式识别受体（pattern recognition receptors，PRRs）如Toll样受体（Toll like receptors，TLRs）可激活胞内信号通路，诱导免疫相关基因和促炎基因的表达，进而启动炎症反应及抗病毒应答，参与乙型肝炎重症化的发生和发展。
2.肝脏聚集了包括自然杀伤（natural killer，NK）细胞、自然杀伤T淋巴细胞（natural killer T cells，NKT cells）、巨噬细胞、中性粒细胞、γδT淋巴细胞、黏膜相关恒定T淋巴细胞（mucosal associated invariant T cells，MAIT cells）、肝窦内皮细胞（liver sinusoidal endothelial cell，LSEC）等在内的大量固有免疫细胞，它们可通过直接细胞毒效应、分泌抗病毒细胞因子和促炎分子等形成抵御病毒感染的早期防线，还能够通过调节特异性免疫应答参与乙型肝炎重症化的发生和发展。
3.适应性免疫应答的特异性及反应强度与病毒感染的临床结局密切相关。在乙型肝炎重症化进程中，患者表现为抗原特异性CTLs的细胞应答失调，T淋巴细胞亚群免疫平衡紊乱和B淋巴细胞耗竭，肝内亦常伴有大量非特异性炎性细胞浸润、肝细胞不同死亡方式的激活等现象。
4.肝脏门静脉血液富含肠道来源微生物产物及食物组分，使得肝脏成为机体最早、最常接触病原体等异源物质的器官。正常生理状态下，肝脏可选择性忽略上述异源物质刺激，以维持自身稳态。肝脏接触肠道来源的病原体等异物时，机体通过精确的调节而区分“自己”与“非己”，从而维持肝脏稳态并确保其功能正常发挥，实现对自身抗原的耐受及对病原体等异物的清除。固有免疫在上述过程中发挥重要作用。
5.肝脏是凝血因子、抗凝蛋白以及纤溶系统蛋白合成及代谢的重要场所，病毒因素直接上调或通过上游炎性通路激活fgl2凝血酶原酶所致的肝脏微循环障碍、肝脏损伤导致的外周循环凝血功能紊乱是乙型肝炎重症化/肝衰竭进展的重要机制。
6.早期抗病毒治疗的实施不仅能够抑制病毒的复制，也有利于机体免疫功能的平衡，可有效遏制乙型肝炎重症化的疾病进程。
As an important immune organ,liverhas a great effect on determining the prognosis of severehepatitis B/liver failure mainly by modulating antiviral immune response and maintaining the balance between coagulation system and anticoagulant system.
1.As the first sensor to recognize HBV and its products, PRRs （e.g.TRLs） induce the expression of immune-associated genes and proinflammatory genes by activating intracellular signal transduction pathways. These pathways induce inflammatory and anti-viral responses that affect the development of severehepatitis B.
2.The liver is an important immune organ with large numbers of innate immune cells, including NK cells, NKT cells, macrophages, neutrophils, γδT lymphocytes, MAIT cells and LSEC. These cells are crucial for early defences against viral infection through direct cytotoxic effect and production of antiviral and proinflammatory cytokines. In addition, these cells participate in the progression of severehepatitis B by initiating specific immune responses.
3.Clinical outcomes of viral infection are closely related to the specificity and intensity of specific immune responses. During the development of severehepatitis B, thehost immune response is characterized by the dysfunction of antigen specific CTLs, imbalance of T lymphocyte subsets, and exhuastion of B lymphocytes.Large numbers of infiltrated non-specific inflammatory cells and apoptosis ofhepatocytes were also observed in liver tissue from patients.
4.Liver is the organ where the body first and most continuously exposed to pathogens and otherheterologous substances, for the blood inhepatic portal vein contains large amount of intestinal microbial products and food components. In physiological conditions, the liver can selectively ignore the stimulation ofheterologous substances to maintainhomeostasis. When the liver is exposed to pathogens and otherheterologous substances from the intestine, the body can distinguish between self and non-self by accurate regulation, maintaining the liverhomeostasis and function, realizing the tolerance to self antigens and clearance of pathogens. Innate immunity plays an crucial role in the processes above.
5.Most coagulation factors, anticoagulant proteins and components of the fibrinolytic system are synthesized and cleared in the liver. Fgl2 prothrombinase pathway could be activated by viral factors or upstream proinflammatory signals, resulting in the disorder of microcirculation, together with the peripheral circulation dysfunction induced by the impaired liver function, are regarded as the important mechanisms in the development of severehepatitis B/liver failure.
6.Early antiviral treatment can not only inhibit virus replication, but alsohelp in the recovery ofhost immunity.It may inhibit the exacerbation of severehepatitis B.