Background/Aim: TGF-β expression is increased in immune-mediated and fibrotic renal diseases and modulates the tubulointerstitial T-cell response. We examined whether TGF-β changes the expression of PD-L1 and CD40 in the renal proximal tubular epithelial cell (TEC), and whether the activation of CD8<sup>+</sup> cytotoxic T cells (CTLs) is influenced by TGF-β treatment of TECs. Methods: Murine TECs were treated with TGF-β or IFN-γ. The expression of PD-L1 and CD40 was examined with RT-PCR and flow cytometry. To investigate if TGF-β treatment influenced the antigen presentation capacity of TECs, OT-1 CTLs were co-incubated with TGF-β-treated, OVA<sub>257–264</sub> peptide-pulsed congeneic TECs. The cytotoxicity of OT-1 CTLs was estimated by their capacity to produce IFN-γ and their cytolytic activity. Results: TGF-β treatment lead to a transition in morphology of renal TECs and downregulated the basal and the IFN-γ-stimulated PD-L1 expression in TECs. Interestingly, TGF-β treatment of TECs increased the constitutive and IFN-γ-induced CD40 expression. In contrast to IFN-γ which reduced the CTL activity, TGF-β treatment of TECs elevated the OVA-specific CTL response. Conclusion: Our data show that TGF-β changed the cellular phenotype and the expression of PD-L1 and CD40 on TECs and enhanced the activity of OVA peptide-specific CD8<sup>+</sup> T cells. TGF-β may thereby play an important role in the progression of renal tubulointerstitial damage in CD8<sup>+</sup> T-cell-mediated renal diseases.