TLR2-deficient mice exacerbated renal injury in cisplatin-induced AKI, with higher serum creatinine and blood urea nitrogen, more severe morphological injury compared with that of wild-type mice.
Adoptive transfer of TLR-2-primed WTDCs significantly expanded Tregs in the kidneys of CDDP-treated WT and Gal-3<sup>-/-</sup> recipients resulting in the suppression of IFN-γ and IL-17-driven inflammation and alleviation of AKI.