Importantly, genetic deletion or pharmacological inhibition of Gal-3 completely diminished capacity of WTDCsPam3CSK4 to enhance nephroprotective properties of Tregs, indicating crucially important role of Gal-3 for the crosstalk of TLR-2-primed renal DCs and Tregs in Tregs-based attenuation of CDDP-induced AKI (Figure 9). This evidence concerns the gene TLR2 and acute kidney injury.