<i>In vivo</i>, NK cell-specific <i>TIGIT</i> deletion alleviated hepatic inflammation, collagen deposition, and fibrosis marker expression in schistosomiasis-infected mice.<h4>Conclusion</h4>These findings identify TIGIT as a key negative regulator of NK cell antifibrotic activity and reveal an immunoregulatory TIGIT-interferon-γ-IFI30 axis that drives NK cell dysfunction and promotes schistosomiasis-induced liver fibrosis. Here, TIGIT is linked to Hepatic fibrosis.