%0 journal article
%@ 1724-6059
%A Roch, Toralf,Paniskaki, Krystallenia,Wehler, Patrizia,Thieme, Constantin J.,Moradian, Hanieh,Blazquez-Navarro, Arturo,Anft, Moritz,Reinke, Petra,Westhoff, Timm H.,Stervbo, Ulrik,Babel, Nina
%D 2025
%J Journal of Nephrology

%P -- 
%R doi:10.1007/s40620-025-02298-2
%T Urine-derived renal tubular epithelial cells resemble functional characteristics of professional antigen-presenting cells and can directly induce BKV-specific T cell responses
%U https://doi.org/10.1007/s40620-025-02298-2
 
%X Background: Reactivation of the BK virus (BKV) is a critical adverse event after kidney transplantation and can lead to graft loss. BKV-reactive T cell-mediated viral control can be facilitated by reducing immunosuppression. However, the exact mechanism underlying the T cell-mediated BKV clearance in the kidney transplant is not clear.
Methods: Here, we used urine-derived renal tubular epithelial cells as a model system to investigate the immunomodulatory capacity of urine-derived renal tubular epithelial cells and their potential to induce T cell responses against BKV. Urinederived renal tubular epithelial cells were generated by culturing urine-derived cell pellets. To assess the inflammatory potential of urine-derived renal tubular epithelial cells, the cells were treated with Poly I:C or TNFα/IFNγ. To investigate urine-derived renal tubular epithelial cell-induced T cell responses, autologous T cells, isolated from blood were co-cultured with urine-derived renal tubular epithelial cells, in the presence of BKV protein-derived peptides and PolyI:C or TNFα/ IFNγ. BKV-reactive T cells,  ytokine/chemokine secretion and expression of co-stimulatory molecules were evaluated using multiplex  ssays and multi-parameter flow cytometry.