In summary, our findings indicated that Th17 responses is one of the promotor driving fibrosis in schistosomiasis in addition to Th2 responses, and emphasizedthat ICOSL/ICOS signaling mediates the IL-17-producing CD4+ T cell response which could contribute to severe hepatic granulomatous inflammation and subsequent fibrosis via Th17. This evidence concerns the gene CD4 and schistosomiasis.