Th17 cells and Th1 cells coordinate to play a critical role in the formation of inflammatory bowel diseases. To examine how Th17 and Th1 cells are regulated at inflammatory sites, we used Th1-dominant CD4+CD45RBhigh T cell-transferred RAG-2−/− and Th1/Th17-mixed IL-10−/− mice. Interestingly, not only did colitic RAG-2−/− mice that were parabiosed with WT mice show significant amelioration of colitis, but amelioration of disease was also observed in those parabiosed with colitic IL-10−/− mice. To assess the interference between Th1 and Th17 colitogenic T cells, we co-transferred colitogenic CD4+ T cells from the lamina propria (LP) of CD4+CD45RBhigh T cell-transferred RAG-2−/− mice and IL-10−/− mice into RAG-2−/− mice. Surprisingly, the co-transferred RAG-2−/− mice showed a vast cellular infiltration of LP CD4+ T cells similar to that seen in RAG-2−/− mice re-transferred with the cells from colitic RAG-2−/− mice alone, but the co-transferred RAG-2−/− mice did not have the wasting symptoms, which are also absent in RAG-2−/− mice transferred with cells from colitic IL-10−/− mice alone. Furthermore, the percentages of Th1 and Th17 cells originating from IL-10−/− mice and those of Th1 cells originating from colitic RAG-2−/− mice were all significantly decreased in the co-transferred mice as compared with the singly-transferred paired RAG-2−/− mice, suggesting that Th1 and Th17 cells are in competition, and that their orchestration results in a merged clinical phenotype of the two types of murine colitis.