Triggering receptor expressed on myeloid cells 2 （TREM2） is expressed in resident non-parenchymal cells （NPCs） and is involved in various pathological processes including liver inflammation and immunoregulation. In recent years， TREM2 has attracted attention in the field of acute and chronic liver diseases， and more and more studies have shown that TREM2 is a potential target for the treatment of acute and chronic liver diseases； however， there is a lack of systematic summary for the mechanism of action of TREM2 in acute and chronic liver diseases. Therefore， this article reviews the latest research advances in the regulatory role of TREM2 in acute and chronic liver diseases， in order to provide new ideas for the clinical prevention and treatment of acute and chronic liver diseases.

Fibrosis is one of the key factors that lead to the immune exclusion of solid tumors. Although degradation of fiber is a promising strategy, its application was still bottlenecked by the side effects of causing metastasis, resulting in the failure of immunotherapy. Here, we developed an antimetastatic polymer (HPA) for the delivery of chemo-drug and antifibrotic siPAI-1 to form the nano-permeator. Nano-permeator shrank after protonation and deeply penetrated into the tumor core to down-regulate the expression of PAI-1 for antifibrosis, and further promoted the sustained infiltration and activation of T cells for killing tumor cells. Moreover, metastasis after fiber elimination was prevented by multivalent CXCR4 antagonistic HPA to reduce the attraction of CXCL12 secreted by distant organs. The administration of stroma-alleviated immunotherapy increased the infiltration of CD8⁺ T cells to 52.5% in tumor tissues, inhibiting nearly 90% metastasis by HPA in distant organs. The nano-permeator reveals the mechanism and correlation between antifibrosis and antimetastasis and was believed to be the optimizing immunotherapy for solid fibrotic tumors.