Schistosomiasis is an infectious disease caused by parasitic worms that affects more than 210-million people, predominantly in developing countries. Its main pathological feature is a pro-inflammatory reaction to the parasite eggs that are trapped in tissues or organs, with subsequent formation of hepatic granulomas (nodules of immune cells) and fibrosis, processes against which current treatments are often inefficacious. Recent data showed that the chemokine Cx3cr1, expressed by macrophages, promotes fibrotic processes. Thus, Cong-Yi Wang and colleagues sought to investigate whether reducing Cx3cr1 signalling in infiltrating macrophages can prevent hepatic granulomas in Schistosoma japonicum-infected mice – a well-established model of human schistosomiasis. The group found that S. japonicum infection increased the expression of Cx3cr1 in infiltrating macrophages, whereas lack of the Cx3cr1 gene prevented egg-induced granuloma formation and hepatic injury in the animals. Interestingly, loss of Cx3cr1 induced M2 polarisation of macrophages, a process that enhances the helper-T-cell-2 (Th2) response, a key T-cell-mediated pro-inflammatory reaction against intracellular parasites. These results suggest CX3CR1 as a viable therapeutic target for the treatment of human schistosomiasis. Page 691

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.