TLR2 and acute kidney injury: In order to determine whether Gal-3 and IDO1 are members of the same TLR-2-initiated signaling pathway responsible for DCs-mediated attenuation of CDDP-induced AKI, we inhibited IDO1 activity in Gal-3 deficient TLR-2-primed DCs (Gal-3-/-DCsPam3CSK4+1-MT) and analyzed their nephroprotective and immunosuppressive effects in CDDP-treated WT (Figure 8) and Gal-3-/- recipients (Figure 9).