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Inflammation plays a crucial role in initiating renal fibrosis after injury. The infiltration of inflammatory cells, such as CD4 + T cells and macrophages, contributes to renal fibrosis following ureteric obstruction. However, the function of CD8 + T cells in obstructed kidneys remains unclear. Although CD8 + T cell depletion intensifies renal fibrosis by decreasing IFN-γ and increasing IL-4 in the kidneys, the change and role of CD8 T cell populations following environmental changes during renal fibrosis are largely unknown. Here, we identified two CD8 T cell subsets in mouse obstructed kidneys with unilateral ureteric obstruction and revealed their different functions in building an inflammatory or profibrotic environment. Following renal fibrosis, the phenotypes of infiltrated CD8 T cells were mainly Tc1 (CD44 + CD25 - CD62L - ) at the early inflammation stage and then changed to Tc2 (CD44 + CD25 high CD62L low ). Tc1 and Tc2 secreted IFN-γ, contributing to the decrease in the Th2-induced over-polarization of M2 macrophages and fibrosis. Moreover, Tc2 secreted pro- and anti-inflammation factors and decreased the inflammatory responses of other cells to control inflammation and fibrosis. This work and our previous study showed that CD8 T cells could balance out inflammation by controlling its level in renal fibrosis.