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⁺CD45RB^high 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⁺CD45RB^high 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.