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Substance P (SP) enhances antigen-dependent T cell IFN-[gamma] production. It was determined if a T cell neurokinin-1 receptor (NK-1R) was critical for IFN-[gamma] regulation. T cells from schistosome-infected mice were mixed with splenocytes from uninfected NK-1R knockout (KO) animals. Thus only the schistosome egg antigen-specific T cells expressed NK-1R. The cells were cultured 18 h with or without SP. SP enhanced antigen-induced IFN-[gamma] production fourfold without affecting IL-4 or IL-5 secretion. NK-1R inhibitor blocked this stimulation. Neither purified T cells nor naive KO splenocytes cultured alone responded to antigen. To further define the importance of T cell NK-1R, we developed a T cell-selective NK-1R KO mouse by reconstituting T cell-deficient Rag mice with NK-1R KO T cells. These mice challanged with schistosomiasis developed abnormal liver granulomas. Granuloma size was smaller in T cell-selective NK-1R KO mice compared with granulomas in Rag reconstituted with normal T cells. Splenocytes and granuloma cells from NK-1R KO mice made less IFN-[gamma]. The mice also made less IgG2a. Thus T cell NK-1R is important for IFN-[gamma] regulation. neuropeptides; inflammation; granuloma; neurokinin 1 receptor; schistosomiasis

Tumor necrosis factor (TNF), a cytokine, can produce egg granulomas and the schistosomes, the parasitic worms that cause schistosomiasis, employ host TNF alpha to stimulate reproduction. Researcher P. Amiri and colleagues found that the schistosome pathogens are able to use TNF when T and B lymphocytes, which form part of the body's immune system, are not present. These findings may lead the way to more research on the co-evolution of parasites and host cytokine responses.