Editorial: Parasite-induced liver diseases, volume II

A central theme of this collection is the diversity of immune checkpoint mechanisms that parasites exploit to subvert hepatic immunity. Tang and colleagues mapped hepaticEchinococcus multilocularis (E. multilocularis) infection drives the concurrent expansion of cytotoxic, effector-memory, and exhausted CD8⁺ T-cell subsets, with coordinated upregulation of negative regulatory genes (Btg1, Tnfaip3, Junb, Nr4a1) and downregulation of early inflammatory mediators. These findings align with a growing body of evidence showing that T-cell exhaustion is a hallmark of chronic AE (Yang et al., 2024a). Indeed, recent work has demonstrated that depletion of myeloidderived suppressor cells can restore T-cell function and enhance antiparasitic immunity in AE (Zhang et al., 2024a). Furthermore, Wang and colleagues showed that Tim-4⁺ macrophages, which accumulate in AE lesions, suppress proinflammatory cytokine production and promote immune tolerance. Importantly, inhibition of Tim-4 only restored balance but also reversed hepatic fibrotic progression in vitro, pointing to a dual role for this molecule in immune evasion and remodeling. In