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Schistosomiasis is a water-borne infection caused mainly by human schistosomes including Schistosoma mansoni (S. mansoni) and Schistosoma japonicum (S. japonicum). In the infected host, immune events in the skin appear to have an important initiating role in determining the type, and guiding the magnitude, of the ensuing acquired immune response. The previous studies of S. mansoni showed that dendritic cells (DCs) prime Th2 response after activating with products released by schistosome larvae (material released in the first 3 h after transformation, 0-3hRP). Therefore, it is interesting to know whether 0-3hRP from S. japonicum also activate DC and induce Th2 immune response. Here, we report 0-3hRP of S. japonicum failed to stimulate the maturation of bone marrow-derived DCs (BM-DCs), while soluble antigen of the body of cercariae preparation (SCAP) induced BM-DCs to mature which can be weakened by 0-3hRP. Moreover, using an in vitro ovalbumin peptide-restricted priming assay, DCs treated with 0-3hRP failed to induce T cells to secrete more cytokines than the negative control group by CD4(+) T cells from DO11.10 transgenic mice, while DCs treated with SCAP upregulated secretions of IFN-γ and IL-17A, but downregulated IL-4. Importantly, BM-DCs treated with 0-3hRP plus SCAP induced BM-DCs selective mature which drive Th2-type polarized response. Our in vitro results agree with the findings of in vivo studies by inoculation of DO11.10 mice with different stimulus-activated DCs pulsed with ovalbumin peptide. Our data demonstrate that the secretions from invading cercariae of S. japonicum (0-3hRP) impaired DCs to mature, which is potentially allowing the parasite to negotiate the immune recognition and attack.

The secretions products from invading cercariae of S. japonicum (0–3hRP) restrain mouse dendritic cells to mature