Research Progress on the Mechanism of Th1/Th2 Immune Response Imbalance in Hepatic Multilocular Echinococcosis

Abstract

Hepatic multilocular echinococcosis (Em) is a parasitic disease caused by infection with Echinococcus multilocularis (Em). Its pathological characteristics are that the lesion is composed of vesicles with a diameter of millimeters, which grow and proliferate in the liver, forming a central liquefaction necrosis and patchy calcification, with liver tissue infiltrating the “lesion” [1]. Research has found that Echinococcus can survive and proliferate in the host’s body for a long time, highly dependent on its ability to evade host immune surveillance and attacks. By actively regulating the host’s immune response, it gradually forms a series of complex and sophisticated immune regulatory mechanisms [2]. At present, it is believed that the immune evasion response caused by hepatic echinococcosis is closely related to the mutual regulation of Th cells and their secreted cytokines. The research results of Rigano et al. indicate that the imbalance of Th1/Th2 immune response plays an important role in the immune response to hydatid infection [3]. This study elucidates the immune regulatory mechanism of hepatic multilocular echinococcosis, with a focus on the central role of Th cell-mediated immune response imbalance in the occurrence and development of the disease.