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Background Type 2 cytokine interleukin (IL)-13 and its decoy receptor, IL-13 receptor (R)α2 appear to play a major role in tissue fibrosis of schistosomiasis and asthma. IL-13 is a key regulator of the extracellular matrix (ECM). It is known to signal to cells by binding to the IL-13Ra1, which then heterodimerizes with IL-4Rα. In contrast, IL-13Rα2 binds IL-13 with high affinity but does not signal. IL-13Rα2 is known to down-regulate granulomatous inflammation and prolong host survival in Schistosoma mansoni (S. Mansoni) infection, but little is known about the location and expression level of IL-13Ra2 in the context of S. Japonicum infection. Methods We established S. Japonicum-infected mouse models. Kinetic serum levels of IL-13Rα2 were examined with ELISA. IL-13Rα2 mRNA and protein of liver tissues were determined by PCR and immunoblotting analysis, respectively. Detection of IL-13Rα2 expression and location in macrophages was performed by TaqMan PCR and fluorescent immunocytochemistry technique, respectively. Results A marked elevation of mRNA and protein expression of IL-13Rα2 was observed in mice during S. Japonicum infection. An enhanced expression of IL-13Rg2 was further demonstrated in primary macrophages of murine schistosomiasis. Conclusions IL-13Rα2 in macrophages may be a critical contributor to pathogenesis of schistosomiasis. The data highlight the potential importance of cell signaling and antifibrotic gene therapeutics in T helper 2 cell (Th2)-mediated diseases.