Characteristics of Schistosoma japonicum infection induced IFN-γ and IL-4 co-expressing plasticity Th cells

Schistosoma japonicum infection can induce granulomatous inflammation and cause tissue damage in the mouse liver. The cytokine secretion profile of T helper (Th) cells depends on both the nature of the activating stimulus and the local microenvironment (e.g. cytokines and other soluble factors). In the present study, we found an accumulation of large numbers of IFN-+IL-4(+)CD4(+) T cells in mouse livers. This IFN-+IL-4(+) cell population increased from 068 +/- 057% in uninfected mice to 705 +/- 30% by week 4 following infection and to 96 +/- 528% by week 6, before decreasing to 63 +/- 59% by week 8 in CD4 T cells. Moreover, IFN-+IL-4(+) Th cells were also found in mouse spleen and mesenteric lymph nodes 6weeks after infection. The majority of the IFN-+IL-4(+) Th cells were thought to be related to a state of immune activation, and some were memory Tcells. Moreover, we found that these S.japonicum infection-induced IFN-+IL-4(+) cells could express interleukin-2 (IL-2), IL-9, IL-17 and high IL-10 levels at 6weeks after S.japonicum infection. Taken together, our data suggest the existence of a population of IFN-+IL-4(+) plasticity effector/memory Th cells following S.japonicum infection in C57BL/6 mice.