Research Paper Volume 12, Issue 17 pp 17528—17540

Figure 6. Model summarizing the role of CD8 T cells in renal inflammation and fibrosis response to UUO. During the process of renal fibrosis, two subsets of CD8 T cells collaborate with each other to control the progression of inflammation from proinflammation to anti-inflammation and avoid excessive renal fibrosis. The transformation of Tc1 cells to Tc2 cells facilitates the conversion of proinflammation to anti-inflammation after renal injury (1). Tc1 and Tc2 cells secrete INF-γ to inhibit the differentiation of Th2 cells and to prevent the Th2 cell-induced excessive polarization of M2 cells (2). The anti-inflammatory factors secreted by Tc2 cells can also promote the polarization of M2 cells. M2 cells further participate in the construction of a profibrotic environment (3). CD8 T cell depletion results in the accumulation of Th2 cells (4), leading to the excessive polarization of M2 cells, which further exacerbates renal fibrosis (5).