In human intermediate hosts, it drives the initiation and progression of CE through two mechanisms: first, inducing a Th2-biased immune response (suppression of pro-inflammatory cytokines and upregulation of IL-10); second, exerting dual regulation of cell death pathways—promoting apoptosis while inhibiting the release of pyroptosis-related inflammatory factors—thereby enabling the “silent” elimination of immune cells and ensuring the long-term survival of larval cysts. Here, IL10 is linked to cholesteryl ester measurement.